unique_id,web-scraper-start-url,sub_chapters_x,sub_chapters-href,paragraph,is_paragraph,sub_section_headings,fig_num,sub_chapters_y,images-src,image_caption
8c8ab993-ee48-4ae5-8847-bcbf32f47061,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,,Figure 7.1,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
8c8ab993-ee48-4ae5-8847-bcbf32f47061,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,,Figure 7.1,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
8c8ab993-ee48-4ae5-8847-bcbf32f47061,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,,Figure 7.1,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
8c8ab993-ee48-4ae5-8847-bcbf32f47061,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,,Figure 7.1,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
8c8ab993-ee48-4ae5-8847-bcbf32f47061,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,,Figure 7.1,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
9d4e0880-9f21-484f-b9ac-c6ff8fb556de,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,Types of Myocardial Ischemia and Infarction,False,Types of Myocardial Ischemia and Infarction,,,,
64d10d2a-fd9c-41bb-b48e-727607b9ad2b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The degree of occlusion caused by the plaque and the oxygen demand of the myocardium determine the degree of ischemia that can develop. Arterial occlusion tends not to be a significant factor until the lumen is occluded by about 70 percent. Vascular occlusion may also be masked by formation of anastomoses (new vessels that bypass the occlusion). Rupture of the plaque and formation of a thrombus can drastically and quickly reduce the lumen and blood flow. The degree and duration of ischemia determine the type of acute coronary syndrome that occurs and the clinical impact. Mild or brief ischemia can lead to angina pectoris with no permanent tissue damage, but when ischemia is prolonged then myocardial infarction becomes more likely, and significant changes in ECG and release of cardiac enzymes are seen.",True,Types of Myocardial Ischemia and Infarction,,,,
24600c4f-2ccc-4588-8d18-94cee47e02d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,Stable and unstable angina pectoris,False,Stable and unstable angina pectoris,,,,
693aa8ee-fda5-45f0-873f-67576411c6e8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"While not considered an acute coronary syndrome, stable angina is pain associated with periods of myocardial ischemia, usually associated with exertion and an increase in myocardial oxygen demand that is unmeet because of insufficient tissue perfusion. The inadequate perfusion is most commonly caused by coronary artery disease (vessel occlusion). Stable angina is predictable and regular, and resolves when the myocardial oxygen demand is reduced (i.e., cessation of exercise).",True,Stable and unstable angina pectoris,,,,
ee5d9eca-b1b8-42c6-9ff8-03bb70da5bec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"Unstable angina is more serious and may be an unpredictable exacerbation of anginal pain that had previously been stable. It may occur at rest or lower than usual levels of exertion. Unstable angina is part of the acute coronary syndrome spectrum and may reflect rupture of a plaque that has led to thrombosis. The ECG in unstable angina may show hyperacute T-waves, flattening of the T-waves, inverted T-waves, and ST depression. Without the presence of myocardial damage, unstable angina is not associated with elevated cardiac enzymes (e.g., troponin). Continued or worsening stenosis of the coronary artery leads to tissue infarction and more clinically significant elements of acute coronary syndrome.",True,Stable and unstable angina pectoris,,,,
fff7764f-ceb1-4df7-bcb2-42206013871e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,Non-ST segment elevation myocardial infarction,False,Non-ST segment elevation myocardial infarction,,,,
2395eb07-d28a-4e14-983c-126fe6e1985e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
2395eb07-d28a-4e14-983c-126fe6e1985e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
2395eb07-d28a-4e14-983c-126fe6e1985e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
2395eb07-d28a-4e14-983c-126fe6e1985e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
2395eb07-d28a-4e14-983c-126fe6e1985e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
e88f6f73-35ba-4543-850d-bde4573e3e48,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,Troponin,False,Troponin,,,,
4f0f9ab6-657f-4aef-89da-6fd69fe98608,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"Troponin I is a normal protein important in the contractile apparatus of the cardiac myocyte. It is released into the circulation about three to four hours after MI and are still detectable for ten days afterward. The long half-life allows for the late diagnosis of MI but makes it difficult to detect reinfarction (a major complication associated with new thrombus formation during stent placement). Although there are a number causes for troponin elevation unrelated to MI, troponin elevation is much more sensitive and specific than myoglobin and even creatine kinase.",True,Troponin,,,,
4c70078b-6929-461d-a32c-5da9ed2e8626,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,ST segment elevation myocardial infarction,False,ST segment elevation myocardial infarction,,,,
3cf60f09-5ee1-4aaa-9b08-339066533313,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"ST segment elevation myocardial infarction (STEMI) most often results from complete occlusion of a major epicardial vessel. The resultant myocardial infarction raises cardiac enzymes measured in the blood (as with NSTEMI), but is accompanied by an ST segment elevation on the 12-lead ECG. This is the most serious of the acute coronary syndromes.",True,ST segment elevation myocardial infarction,,,,
e78b3de3-d87d-4158-9f50-e4a2516402ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,Pathophysiology of a STEMI,False,Pathophysiology of a STEMI,,,,
0f262d19-ab49-437d-87c8-88681d2af370,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The most common cause of a STEMI is rupture of an atherosclerotic plaque. The continued degradation and calcification of the fibrous cap results in it breaking and spilling its contents into the bloodstream. Tissue factor within the necrotic core instigates the coagulation cascade when it is exposed to the blood and a thrombus is formed and the vessel is occluded. Plaques rupture most frequently at their “shoulder,” the thin peripheral edges where proteolytic and apoptotic activity are highest and mechanical forces are most effective. The tissue downstream from the occlusion experiences ischemia and then infarcts. The impact on cardiac function and output depends on the site and extent of the infarcted tissue. For example, if a significant section of the left ventricular wall is involved, then the fall in cardiac output may be catastrophic, or if the papillary muscles of a valve are included, the valve may become incompetent and allow regurgitation.",True,Pathophysiology of a STEMI,,,,
92596e8c-cd79-4c33-9b0f-18249fb0c967,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,Physical Exam of a STEMI,False,Physical Exam of a STEMI,,,,
99654ea9-1084-45f3-8c5b-2479b32f7b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
99654ea9-1084-45f3-8c5b-2479b32f7b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
99654ea9-1084-45f3-8c5b-2479b32f7b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
99654ea9-1084-45f3-8c5b-2479b32f7b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
99654ea9-1084-45f3-8c5b-2479b32f7b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
a75a7fe1-ec08-4354-b08d-c7acfbfd7914,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,Diagnosis of a STEMI,False,Diagnosis of a STEMI,,,,
d23a054f-12c2-4916-b9b0-6ca0f924a9fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
d23a054f-12c2-4916-b9b0-6ca0f924a9fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
d23a054f-12c2-4916-b9b0-6ca0f924a9fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
d23a054f-12c2-4916-b9b0-6ca0f924a9fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
d23a054f-12c2-4916-b9b0-6ca0f924a9fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
ba2ac968-c97b-41e2-b754-9f1afe1b868d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,Changes in ECG,False,Changes in ECG,,,,
72ffb72c-4a64-4cc6-873f-de27f4b99bc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
72ffb72c-4a64-4cc6-873f-de27f4b99bc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
72ffb72c-4a64-4cc6-873f-de27f4b99bc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
72ffb72c-4a64-4cc6-873f-de27f4b99bc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
72ffb72c-4a64-4cc6-873f-de27f4b99bc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
88db4132-68ca-4549-89a2-924cf9f900ea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
88db4132-68ca-4549-89a2-924cf9f900ea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
88db4132-68ca-4549-89a2-924cf9f900ea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
88db4132-68ca-4549-89a2-924cf9f900ea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
88db4132-68ca-4549-89a2-924cf9f900ea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
6d68f09a-8787-48f2-b06c-14d0b66cf653,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,Anterior wall myocardial infarctions (AWMI),False,Anterior wall myocardial infarctions (AWMI),,,,
49edadfd-c220-471a-a2a7-98961115d828,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
49edadfd-c220-471a-a2a7-98961115d828,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
49edadfd-c220-471a-a2a7-98961115d828,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
49edadfd-c220-471a-a2a7-98961115d828,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
49edadfd-c220-471a-a2a7-98961115d828,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
986cf8b1-e6e2-4571-8ae3-2049c903e560,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,Inferior wall myocardial infarction (IWMI),False,Inferior wall myocardial infarction (IWMI),,,,
6bffe156-b418-440d-b656-519ab719029a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
6bffe156-b418-440d-b656-519ab719029a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
6bffe156-b418-440d-b656-519ab719029a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
6bffe156-b418-440d-b656-519ab719029a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
6bffe156-b418-440d-b656-519ab719029a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
2aecae86-a90c-4fa9-8f1e-b688c1a0e472,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,Posterior wall myocardial infarction (PWMI),False,Posterior wall myocardial infarction (PWMI),,,,
efe18db6-82d6-407b-ac2b-58efb88e6c6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
efe18db6-82d6-407b-ac2b-58efb88e6c6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
efe18db6-82d6-407b-ac2b-58efb88e6c6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
efe18db6-82d6-407b-ac2b-58efb88e6c6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
efe18db6-82d6-407b-ac2b-58efb88e6c6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
c3555430-b628-4c1d-a1b4-ea3410d63415,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"The location of the infarction, leads showing ST elevation and depression, and the involved coronary artery are summarized in table 7.1.",True,Posterior wall myocardial infarction (PWMI),,,,
fad9a2c1-10a1-4b64-b8df-f054450efa3c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"Table 7.1: Location of the infarction, leads showing ST elevation and depression, and the involved coronary artery.",True,Posterior wall myocardial infarction (PWMI),,,,
2651f059-9715-43df-b265-f410f3408493,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,Text,False,Text,,,,
8c6e0429-e47f-4997-a67a-ddf069d958f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"Rhee, June-Wha, Sabatine, Marc S., and Leonard S. Lilly. “Ischemic Heart Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e, edited by Leonard S. Lilly, Chapter 6. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
f418f90a-4b61-47fe-9986-92500c9a8db6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"Rhee, June-Wha, Sabatine, Marc S., and Leonard S. Lilly. “Acute Coronary Syndromes.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e, edited by Leonard S. Lilly, Chapter 7. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
0d5c9a9d-0b35-43ee-a67d-f78f5b489c22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"Surawicz, Borys, Rory Childers, Barbara J. Deal, and Leonard S. Gettes. “AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram.” Circulation 119, no. 10 (2009): e235–e240.",True,Text,,,,
60ff9e9a-c126-471e-99f6-c12310ca27fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-4,"Surawicz, Borys, and Timothy Knilans. Chou’s Electrocardiography in Practice, 6th ed. Philadelphia: Saunders, 2008.",True,Text,,,,
5ab0ae7c-0897-40a5-acac-c2c15ceaba54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,Text,Figure 7.1,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
5ab0ae7c-0897-40a5-acac-c2c15ceaba54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,Text,Figure 7.1,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
5ab0ae7c-0897-40a5-acac-c2c15ceaba54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,Text,Figure 7.1,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
5ab0ae7c-0897-40a5-acac-c2c15ceaba54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,Text,Figure 7.1,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
5ab0ae7c-0897-40a5-acac-c2c15ceaba54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,Text,Figure 7.1,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
8c0de3aa-aeaf-4c7e-aaa3-f164f462697e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,Types of Myocardial Ischemia and Infarction,False,Types of Myocardial Ischemia and Infarction,,,,
2a84f547-2c33-4f1f-8dad-9990925fe831,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The degree of occlusion caused by the plaque and the oxygen demand of the myocardium determine the degree of ischemia that can develop. Arterial occlusion tends not to be a significant factor until the lumen is occluded by about 70 percent. Vascular occlusion may also be masked by formation of anastomoses (new vessels that bypass the occlusion). Rupture of the plaque and formation of a thrombus can drastically and quickly reduce the lumen and blood flow. The degree and duration of ischemia determine the type of acute coronary syndrome that occurs and the clinical impact. Mild or brief ischemia can lead to angina pectoris with no permanent tissue damage, but when ischemia is prolonged then myocardial infarction becomes more likely, and significant changes in ECG and release of cardiac enzymes are seen.",True,Types of Myocardial Ischemia and Infarction,,,,
04d4586f-524e-4835-b734-ca06d13913c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,Stable and unstable angina pectoris,False,Stable and unstable angina pectoris,,,,
22b0b56a-8e6f-43ee-a88c-656ebd8000c1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"While not considered an acute coronary syndrome, stable angina is pain associated with periods of myocardial ischemia, usually associated with exertion and an increase in myocardial oxygen demand that is unmeet because of insufficient tissue perfusion. The inadequate perfusion is most commonly caused by coronary artery disease (vessel occlusion). Stable angina is predictable and regular, and resolves when the myocardial oxygen demand is reduced (i.e., cessation of exercise).",True,Stable and unstable angina pectoris,,,,
92c6d912-d723-4c88-92fc-68e29b1214ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"Unstable angina is more serious and may be an unpredictable exacerbation of anginal pain that had previously been stable. It may occur at rest or lower than usual levels of exertion. Unstable angina is part of the acute coronary syndrome spectrum and may reflect rupture of a plaque that has led to thrombosis. The ECG in unstable angina may show hyperacute T-waves, flattening of the T-waves, inverted T-waves, and ST depression. Without the presence of myocardial damage, unstable angina is not associated with elevated cardiac enzymes (e.g., troponin). Continued or worsening stenosis of the coronary artery leads to tissue infarction and more clinically significant elements of acute coronary syndrome.",True,Stable and unstable angina pectoris,,,,
ee1ddb15-d45d-41c4-a288-5772b25a27b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,Non-ST segment elevation myocardial infarction,False,Non-ST segment elevation myocardial infarction,,,,
1dab5ea9-b0eb-45bf-944a-864e815d2850,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
1dab5ea9-b0eb-45bf-944a-864e815d2850,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
1dab5ea9-b0eb-45bf-944a-864e815d2850,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
1dab5ea9-b0eb-45bf-944a-864e815d2850,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
1dab5ea9-b0eb-45bf-944a-864e815d2850,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
95cf9910-95a9-406a-9415-57ba3c82e748,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,Troponin,False,Troponin,,,,
a1e8accf-43d0-447f-8255-e92027343c86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"Troponin I is a normal protein important in the contractile apparatus of the cardiac myocyte. It is released into the circulation about three to four hours after MI and are still detectable for ten days afterward. The long half-life allows for the late diagnosis of MI but makes it difficult to detect reinfarction (a major complication associated with new thrombus formation during stent placement). Although there are a number causes for troponin elevation unrelated to MI, troponin elevation is much more sensitive and specific than myoglobin and even creatine kinase.",True,Troponin,,,,
0f693c59-73f2-4669-bdc9-eeb51f7aa0a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,ST segment elevation myocardial infarction,False,ST segment elevation myocardial infarction,,,,
78e83aa8-5570-45f8-9c33-3ad4a159287c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"ST segment elevation myocardial infarction (STEMI) most often results from complete occlusion of a major epicardial vessel. The resultant myocardial infarction raises cardiac enzymes measured in the blood (as with NSTEMI), but is accompanied by an ST segment elevation on the 12-lead ECG. This is the most serious of the acute coronary syndromes.",True,ST segment elevation myocardial infarction,,,,
bf80efa7-c138-43ca-849a-48faa2df9d22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,Pathophysiology of a STEMI,False,Pathophysiology of a STEMI,,,,
a709775d-df5f-4939-967e-1022e2ea74be,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The most common cause of a STEMI is rupture of an atherosclerotic plaque. The continued degradation and calcification of the fibrous cap results in it breaking and spilling its contents into the bloodstream. Tissue factor within the necrotic core instigates the coagulation cascade when it is exposed to the blood and a thrombus is formed and the vessel is occluded. Plaques rupture most frequently at their “shoulder,” the thin peripheral edges where proteolytic and apoptotic activity are highest and mechanical forces are most effective. The tissue downstream from the occlusion experiences ischemia and then infarcts. The impact on cardiac function and output depends on the site and extent of the infarcted tissue. For example, if a significant section of the left ventricular wall is involved, then the fall in cardiac output may be catastrophic, or if the papillary muscles of a valve are included, the valve may become incompetent and allow regurgitation.",True,Pathophysiology of a STEMI,,,,
288b9fcd-f87a-4b9c-97be-3a080f7153cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,Physical Exam of a STEMI,False,Physical Exam of a STEMI,,,,
5ece801e-f1c8-4e2b-89ef-8ab4cd189ca5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
5ece801e-f1c8-4e2b-89ef-8ab4cd189ca5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
5ece801e-f1c8-4e2b-89ef-8ab4cd189ca5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
5ece801e-f1c8-4e2b-89ef-8ab4cd189ca5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
5ece801e-f1c8-4e2b-89ef-8ab4cd189ca5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
878abb44-f160-4e30-b344-f9ce70a26c5a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,Diagnosis of a STEMI,False,Diagnosis of a STEMI,,,,
bba89964-9740-4f46-aade-af16023c92fd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
bba89964-9740-4f46-aade-af16023c92fd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
bba89964-9740-4f46-aade-af16023c92fd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
bba89964-9740-4f46-aade-af16023c92fd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
bba89964-9740-4f46-aade-af16023c92fd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
8f0a5fe0-46ca-4933-8247-200439816311,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,Changes in ECG,False,Changes in ECG,,,,
d418402c-3671-4eb2-bde5-b5dbca51e5e5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
d418402c-3671-4eb2-bde5-b5dbca51e5e5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
d418402c-3671-4eb2-bde5-b5dbca51e5e5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
d418402c-3671-4eb2-bde5-b5dbca51e5e5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
d418402c-3671-4eb2-bde5-b5dbca51e5e5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
03c11eea-1c34-42f4-b433-900644e48888,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
03c11eea-1c34-42f4-b433-900644e48888,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
03c11eea-1c34-42f4-b433-900644e48888,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
03c11eea-1c34-42f4-b433-900644e48888,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
03c11eea-1c34-42f4-b433-900644e48888,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
7fb660de-09c5-4505-9b1b-ebf7b4f3f80b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,Anterior wall myocardial infarctions (AWMI),False,Anterior wall myocardial infarctions (AWMI),,,,
c17c6351-52ee-4ca1-b8fe-403cfb987c38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
c17c6351-52ee-4ca1-b8fe-403cfb987c38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
c17c6351-52ee-4ca1-b8fe-403cfb987c38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
c17c6351-52ee-4ca1-b8fe-403cfb987c38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
c17c6351-52ee-4ca1-b8fe-403cfb987c38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
9200e50e-0bbf-464c-ad5b-31de21934220,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,Inferior wall myocardial infarction (IWMI),False,Inferior wall myocardial infarction (IWMI),,,,
459057e1-4d5b-415b-b188-5fcde3579601,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
459057e1-4d5b-415b-b188-5fcde3579601,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
459057e1-4d5b-415b-b188-5fcde3579601,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
459057e1-4d5b-415b-b188-5fcde3579601,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
459057e1-4d5b-415b-b188-5fcde3579601,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
b2283654-a382-4088-a4cc-056a35197a4f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,Posterior wall myocardial infarction (PWMI),False,Posterior wall myocardial infarction (PWMI),,,,
c438324b-88cf-440f-b56c-db688021e192,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
c438324b-88cf-440f-b56c-db688021e192,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
c438324b-88cf-440f-b56c-db688021e192,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
c438324b-88cf-440f-b56c-db688021e192,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
c438324b-88cf-440f-b56c-db688021e192,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
d528eb8d-17cf-40ea-8b66-18128b14badb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"The location of the infarction, leads showing ST elevation and depression, and the involved coronary artery are summarized in table 7.1.",True,Posterior wall myocardial infarction (PWMI),,,,
3b7a0e17-a9f9-47da-b9c4-9e569bcc4008,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"Table 7.1: Location of the infarction, leads showing ST elevation and depression, and the involved coronary artery.",True,Posterior wall myocardial infarction (PWMI),,,,
52200fb1-b960-4913-9c5b-8064e84b82d8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,Text,False,Text,,,,
c9cfcfc2-cbe1-419d-96c0-9ab808b23445,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"Rhee, June-Wha, Sabatine, Marc S., and Leonard S. Lilly. “Ischemic Heart Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e, edited by Leonard S. Lilly, Chapter 6. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
d4e25cfd-0978-4b07-8a3e-92ba4b28f7c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"Rhee, June-Wha, Sabatine, Marc S., and Leonard S. Lilly. “Acute Coronary Syndromes.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e, edited by Leonard S. Lilly, Chapter 7. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
65af299d-c9b2-4fdc-b3b5-52fc62a2d760,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"Surawicz, Borys, Rory Childers, Barbara J. Deal, and Leonard S. Gettes. “AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram.” Circulation 119, no. 10 (2009): e235–e240.",True,Text,,,,
addb3ed2-36a7-43a8-957e-c6cde6c7d095,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-3,"Surawicz, Borys, and Timothy Knilans. Chou’s Electrocardiography in Practice, 6th ed. Philadelphia: Saunders, 2008.",True,Text,,,,
deb21b6b-e750-4aa6-a36d-83c7f12a775b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,Text,Figure 7.1,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
deb21b6b-e750-4aa6-a36d-83c7f12a775b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,Text,Figure 7.1,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
deb21b6b-e750-4aa6-a36d-83c7f12a775b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,Text,Figure 7.1,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
deb21b6b-e750-4aa6-a36d-83c7f12a775b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,Text,Figure 7.1,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
deb21b6b-e750-4aa6-a36d-83c7f12a775b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,Text,Figure 7.1,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
44f71907-65ea-4aac-bd70-1fc5d0d96ddc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,Types of Myocardial Ischemia and Infarction,False,Types of Myocardial Ischemia and Infarction,,,,
84a7d1e3-48c3-498b-9db2-413ebfdef7bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The degree of occlusion caused by the plaque and the oxygen demand of the myocardium determine the degree of ischemia that can develop. Arterial occlusion tends not to be a significant factor until the lumen is occluded by about 70 percent. Vascular occlusion may also be masked by formation of anastomoses (new vessels that bypass the occlusion). Rupture of the plaque and formation of a thrombus can drastically and quickly reduce the lumen and blood flow. The degree and duration of ischemia determine the type of acute coronary syndrome that occurs and the clinical impact. Mild or brief ischemia can lead to angina pectoris with no permanent tissue damage, but when ischemia is prolonged then myocardial infarction becomes more likely, and significant changes in ECG and release of cardiac enzymes are seen.",True,Types of Myocardial Ischemia and Infarction,,,,
e5b684e5-cd23-4438-8442-3ab64ccf7276,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,Stable and unstable angina pectoris,False,Stable and unstable angina pectoris,,,,
0b952daf-5e58-47af-b700-42cd287650da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"While not considered an acute coronary syndrome, stable angina is pain associated with periods of myocardial ischemia, usually associated with exertion and an increase in myocardial oxygen demand that is unmeet because of insufficient tissue perfusion. The inadequate perfusion is most commonly caused by coronary artery disease (vessel occlusion). Stable angina is predictable and regular, and resolves when the myocardial oxygen demand is reduced (i.e., cessation of exercise).",True,Stable and unstable angina pectoris,,,,
f1957996-fc78-4180-829b-a92033d403d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"Unstable angina is more serious and may be an unpredictable exacerbation of anginal pain that had previously been stable. It may occur at rest or lower than usual levels of exertion. Unstable angina is part of the acute coronary syndrome spectrum and may reflect rupture of a plaque that has led to thrombosis. The ECG in unstable angina may show hyperacute T-waves, flattening of the T-waves, inverted T-waves, and ST depression. Without the presence of myocardial damage, unstable angina is not associated with elevated cardiac enzymes (e.g., troponin). Continued or worsening stenosis of the coronary artery leads to tissue infarction and more clinically significant elements of acute coronary syndrome.",True,Stable and unstable angina pectoris,,,,
0fdf85d3-6f85-4d13-a228-7e6845528773,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,Non-ST segment elevation myocardial infarction,False,Non-ST segment elevation myocardial infarction,,,,
9c528299-3016-4337-b1ee-04cadc9a7042,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
9c528299-3016-4337-b1ee-04cadc9a7042,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
9c528299-3016-4337-b1ee-04cadc9a7042,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
9c528299-3016-4337-b1ee-04cadc9a7042,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
9c528299-3016-4337-b1ee-04cadc9a7042,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
057d7968-239c-41e3-97ef-0294b4d312b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,Troponin,False,Troponin,,,,
29ce1769-ab73-4c46-8240-ca267088ae51,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"Troponin I is a normal protein important in the contractile apparatus of the cardiac myocyte. It is released into the circulation about three to four hours after MI and are still detectable for ten days afterward. The long half-life allows for the late diagnosis of MI but makes it difficult to detect reinfarction (a major complication associated with new thrombus formation during stent placement). Although there are a number causes for troponin elevation unrelated to MI, troponin elevation is much more sensitive and specific than myoglobin and even creatine kinase.",True,Troponin,,,,
058b75ac-d633-43ba-8ddc-84b50d7ff690,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,ST segment elevation myocardial infarction,False,ST segment elevation myocardial infarction,,,,
ed86e2cc-a736-41fa-912f-39277b20c296,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"ST segment elevation myocardial infarction (STEMI) most often results from complete occlusion of a major epicardial vessel. The resultant myocardial infarction raises cardiac enzymes measured in the blood (as with NSTEMI), but is accompanied by an ST segment elevation on the 12-lead ECG. This is the most serious of the acute coronary syndromes.",True,ST segment elevation myocardial infarction,,,,
a8a737f0-5885-49af-a928-140f003f3862,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,Pathophysiology of a STEMI,False,Pathophysiology of a STEMI,,,,
2e0c6a06-2f3b-4bfa-8110-7adf02f48f56,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The most common cause of a STEMI is rupture of an atherosclerotic plaque. The continued degradation and calcification of the fibrous cap results in it breaking and spilling its contents into the bloodstream. Tissue factor within the necrotic core instigates the coagulation cascade when it is exposed to the blood and a thrombus is formed and the vessel is occluded. Plaques rupture most frequently at their “shoulder,” the thin peripheral edges where proteolytic and apoptotic activity are highest and mechanical forces are most effective. The tissue downstream from the occlusion experiences ischemia and then infarcts. The impact on cardiac function and output depends on the site and extent of the infarcted tissue. For example, if a significant section of the left ventricular wall is involved, then the fall in cardiac output may be catastrophic, or if the papillary muscles of a valve are included, the valve may become incompetent and allow regurgitation.",True,Pathophysiology of a STEMI,,,,
36ab2320-4984-4fe0-bd9b-a150876de43d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,Physical Exam of a STEMI,False,Physical Exam of a STEMI,,,,
f661686f-35a7-4bca-aff3-5326eae2341f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
f661686f-35a7-4bca-aff3-5326eae2341f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
f661686f-35a7-4bca-aff3-5326eae2341f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
f661686f-35a7-4bca-aff3-5326eae2341f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
f661686f-35a7-4bca-aff3-5326eae2341f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
4ec83dd4-34b2-4e41-bd21-db8c8da54846,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,Diagnosis of a STEMI,False,Diagnosis of a STEMI,,,,
4bc7f10f-375c-4725-b936-3520b214de9b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
4bc7f10f-375c-4725-b936-3520b214de9b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
4bc7f10f-375c-4725-b936-3520b214de9b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
4bc7f10f-375c-4725-b936-3520b214de9b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
4bc7f10f-375c-4725-b936-3520b214de9b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
ca12b8c8-fd11-4573-b91f-85aae221a140,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,Changes in ECG,False,Changes in ECG,,,,
dc00bda8-4caa-4d9f-bea1-ef2ecd6c4272,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
dc00bda8-4caa-4d9f-bea1-ef2ecd6c4272,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
dc00bda8-4caa-4d9f-bea1-ef2ecd6c4272,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
dc00bda8-4caa-4d9f-bea1-ef2ecd6c4272,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
dc00bda8-4caa-4d9f-bea1-ef2ecd6c4272,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
69456ed0-a197-479e-89c2-ee6599348cc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
69456ed0-a197-479e-89c2-ee6599348cc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
69456ed0-a197-479e-89c2-ee6599348cc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
69456ed0-a197-479e-89c2-ee6599348cc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
69456ed0-a197-479e-89c2-ee6599348cc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
21c7dfd3-1d43-4e84-8750-c8ccfc6f0f4a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,Anterior wall myocardial infarctions (AWMI),False,Anterior wall myocardial infarctions (AWMI),,,,
c0653911-6814-40d9-8ea4-d2b2efd8bdea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
c0653911-6814-40d9-8ea4-d2b2efd8bdea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
c0653911-6814-40d9-8ea4-d2b2efd8bdea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
c0653911-6814-40d9-8ea4-d2b2efd8bdea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
c0653911-6814-40d9-8ea4-d2b2efd8bdea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
fc1659b1-d906-4438-b2b2-fede22b57c3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,Inferior wall myocardial infarction (IWMI),False,Inferior wall myocardial infarction (IWMI),,,,
49d26b28-014b-4113-80e5-53b0a6f5ec72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
49d26b28-014b-4113-80e5-53b0a6f5ec72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
49d26b28-014b-4113-80e5-53b0a6f5ec72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
49d26b28-014b-4113-80e5-53b0a6f5ec72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
49d26b28-014b-4113-80e5-53b0a6f5ec72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
14ae0f06-7b21-4eb4-aee1-817888417797,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,Posterior wall myocardial infarction (PWMI),False,Posterior wall myocardial infarction (PWMI),,,,
19b16916-8206-425d-9685-8a0dbfabcd6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
19b16916-8206-425d-9685-8a0dbfabcd6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
19b16916-8206-425d-9685-8a0dbfabcd6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
19b16916-8206-425d-9685-8a0dbfabcd6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
19b16916-8206-425d-9685-8a0dbfabcd6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
a8000c03-9edd-4099-9d95-f3327c9401c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"The location of the infarction, leads showing ST elevation and depression, and the involved coronary artery are summarized in table 7.1.",True,Posterior wall myocardial infarction (PWMI),,,,
e7deb61a-52ff-4941-bf94-5ba5a1473c47,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"Table 7.1: Location of the infarction, leads showing ST elevation and depression, and the involved coronary artery.",True,Posterior wall myocardial infarction (PWMI),,,,
ace0dced-0987-4999-8f0b-e7a2f9264ad4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,Text,False,Text,,,,
c31d616d-b365-4490-b2f8-adcb27ce9871,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"Rhee, June-Wha, Sabatine, Marc S., and Leonard S. Lilly. “Ischemic Heart Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e, edited by Leonard S. Lilly, Chapter 6. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
87eb9284-ea2a-419d-bc48-b893845eb50a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"Rhee, June-Wha, Sabatine, Marc S., and Leonard S. Lilly. “Acute Coronary Syndromes.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e, edited by Leonard S. Lilly, Chapter 7. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
a6460a58-3abf-4202-aa54-65821f2c0fe1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"Surawicz, Borys, Rory Childers, Barbara J. Deal, and Leonard S. Gettes. “AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram.” Circulation 119, no. 10 (2009): e235–e240.",True,Text,,,,
34316ff4-a805-40ab-becc-19f86540947b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-2,"Surawicz, Borys, and Timothy Knilans. Chou’s Electrocardiography in Practice, 6th ed. Philadelphia: Saunders, 2008.",True,Text,,,,
1d26c301-d93b-440e-82a2-e78c3865c558,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,Text,Figure 7.1,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
1d26c301-d93b-440e-82a2-e78c3865c558,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,Text,Figure 7.1,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
1d26c301-d93b-440e-82a2-e78c3865c558,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,Text,Figure 7.1,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
1d26c301-d93b-440e-82a2-e78c3865c558,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,Text,Figure 7.1,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
1d26c301-d93b-440e-82a2-e78c3865c558,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,Text,Figure 7.1,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
49dc948b-de0b-4fb7-9afd-8c04520870a3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,Types of Myocardial Ischemia and Infarction,False,Types of Myocardial Ischemia and Infarction,,,,
1a57afc1-70d3-4953-ae86-551114b70af8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The degree of occlusion caused by the plaque and the oxygen demand of the myocardium determine the degree of ischemia that can develop. Arterial occlusion tends not to be a significant factor until the lumen is occluded by about 70 percent. Vascular occlusion may also be masked by formation of anastomoses (new vessels that bypass the occlusion). Rupture of the plaque and formation of a thrombus can drastically and quickly reduce the lumen and blood flow. The degree and duration of ischemia determine the type of acute coronary syndrome that occurs and the clinical impact. Mild or brief ischemia can lead to angina pectoris with no permanent tissue damage, but when ischemia is prolonged then myocardial infarction becomes more likely, and significant changes in ECG and release of cardiac enzymes are seen.",True,Types of Myocardial Ischemia and Infarction,,,,
090c3e9b-402a-4241-bdce-7bc70b426a40,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,Stable and unstable angina pectoris,False,Stable and unstable angina pectoris,,,,
9b1dd2b4-1a96-4dc2-8fff-6b6edc970e07,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"While not considered an acute coronary syndrome, stable angina is pain associated with periods of myocardial ischemia, usually associated with exertion and an increase in myocardial oxygen demand that is unmeet because of insufficient tissue perfusion. The inadequate perfusion is most commonly caused by coronary artery disease (vessel occlusion). Stable angina is predictable and regular, and resolves when the myocardial oxygen demand is reduced (i.e., cessation of exercise).",True,Stable and unstable angina pectoris,,,,
13aaa6ab-69d5-4485-9db3-9b81efbc1ae9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"Unstable angina is more serious and may be an unpredictable exacerbation of anginal pain that had previously been stable. It may occur at rest or lower than usual levels of exertion. Unstable angina is part of the acute coronary syndrome spectrum and may reflect rupture of a plaque that has led to thrombosis. The ECG in unstable angina may show hyperacute T-waves, flattening of the T-waves, inverted T-waves, and ST depression. Without the presence of myocardial damage, unstable angina is not associated with elevated cardiac enzymes (e.g., troponin). Continued or worsening stenosis of the coronary artery leads to tissue infarction and more clinically significant elements of acute coronary syndrome.",True,Stable and unstable angina pectoris,,,,
0a20f3ac-7b59-415a-bfba-06d908e129b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,Non-ST segment elevation myocardial infarction,False,Non-ST segment elevation myocardial infarction,,,,
c4588d12-98e7-4208-a906-efc67e84f56d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
c4588d12-98e7-4208-a906-efc67e84f56d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
c4588d12-98e7-4208-a906-efc67e84f56d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
c4588d12-98e7-4208-a906-efc67e84f56d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
c4588d12-98e7-4208-a906-efc67e84f56d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
cdca1052-c35a-42ba-af65-6dabd3189b2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,Troponin,False,Troponin,,,,
c781eb30-67e2-4403-8218-34e547b2e8db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"Troponin I is a normal protein important in the contractile apparatus of the cardiac myocyte. It is released into the circulation about three to four hours after MI and are still detectable for ten days afterward. The long half-life allows for the late diagnosis of MI but makes it difficult to detect reinfarction (a major complication associated with new thrombus formation during stent placement). Although there are a number causes for troponin elevation unrelated to MI, troponin elevation is much more sensitive and specific than myoglobin and even creatine kinase.",True,Troponin,,,,
9d8f86c4-06f4-4c9b-a56d-ff012168ed3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,ST segment elevation myocardial infarction,False,ST segment elevation myocardial infarction,,,,
07b750c7-1e3a-4085-8054-8394da6d1902,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"ST segment elevation myocardial infarction (STEMI) most often results from complete occlusion of a major epicardial vessel. The resultant myocardial infarction raises cardiac enzymes measured in the blood (as with NSTEMI), but is accompanied by an ST segment elevation on the 12-lead ECG. This is the most serious of the acute coronary syndromes.",True,ST segment elevation myocardial infarction,,,,
6cbbbf9a-dea3-4726-8f04-443785620112,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,Pathophysiology of a STEMI,False,Pathophysiology of a STEMI,,,,
aa20af73-1cdf-4e2f-9468-47f19ecc3183,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The most common cause of a STEMI is rupture of an atherosclerotic plaque. The continued degradation and calcification of the fibrous cap results in it breaking and spilling its contents into the bloodstream. Tissue factor within the necrotic core instigates the coagulation cascade when it is exposed to the blood and a thrombus is formed and the vessel is occluded. Plaques rupture most frequently at their “shoulder,” the thin peripheral edges where proteolytic and apoptotic activity are highest and mechanical forces are most effective. The tissue downstream from the occlusion experiences ischemia and then infarcts. The impact on cardiac function and output depends on the site and extent of the infarcted tissue. For example, if a significant section of the left ventricular wall is involved, then the fall in cardiac output may be catastrophic, or if the papillary muscles of a valve are included, the valve may become incompetent and allow regurgitation.",True,Pathophysiology of a STEMI,,,,
3352b3ca-bb3c-4fdf-9efb-397df3f8c292,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,Physical Exam of a STEMI,False,Physical Exam of a STEMI,,,,
7616d9a3-8e18-4b60-a982-6bc7df6410ff,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
7616d9a3-8e18-4b60-a982-6bc7df6410ff,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
7616d9a3-8e18-4b60-a982-6bc7df6410ff,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
7616d9a3-8e18-4b60-a982-6bc7df6410ff,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
7616d9a3-8e18-4b60-a982-6bc7df6410ff,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
05c165b4-063e-4ff5-8383-692a117df7d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,Diagnosis of a STEMI,False,Diagnosis of a STEMI,,,,
7e7a0a42-d28c-41d1-ac5f-48fa5a6fcb8d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
7e7a0a42-d28c-41d1-ac5f-48fa5a6fcb8d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
7e7a0a42-d28c-41d1-ac5f-48fa5a6fcb8d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
7e7a0a42-d28c-41d1-ac5f-48fa5a6fcb8d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
7e7a0a42-d28c-41d1-ac5f-48fa5a6fcb8d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
031528d4-3dc4-4a7e-a018-5848e54ba34b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,Changes in ECG,False,Changes in ECG,,,,
567e15a3-516d-463f-accc-a83a86aef6f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
567e15a3-516d-463f-accc-a83a86aef6f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
567e15a3-516d-463f-accc-a83a86aef6f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
567e15a3-516d-463f-accc-a83a86aef6f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
567e15a3-516d-463f-accc-a83a86aef6f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
8147ec70-9d4c-47a7-9185-e2598d883fc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
8147ec70-9d4c-47a7-9185-e2598d883fc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
8147ec70-9d4c-47a7-9185-e2598d883fc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
8147ec70-9d4c-47a7-9185-e2598d883fc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
8147ec70-9d4c-47a7-9185-e2598d883fc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
0db04f35-e2e1-48f3-b5f0-e2bc1268431a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,Anterior wall myocardial infarctions (AWMI),False,Anterior wall myocardial infarctions (AWMI),,,,
616cd1d0-a502-4870-8311-44f0006559f3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
616cd1d0-a502-4870-8311-44f0006559f3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
616cd1d0-a502-4870-8311-44f0006559f3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
616cd1d0-a502-4870-8311-44f0006559f3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
616cd1d0-a502-4870-8311-44f0006559f3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
e07a1e03-cf58-4015-8c66-82848ff6f9b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,Inferior wall myocardial infarction (IWMI),False,Inferior wall myocardial infarction (IWMI),,,,
075ff635-9f2d-4b19-b4da-734007d4806d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
075ff635-9f2d-4b19-b4da-734007d4806d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
075ff635-9f2d-4b19-b4da-734007d4806d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
075ff635-9f2d-4b19-b4da-734007d4806d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
075ff635-9f2d-4b19-b4da-734007d4806d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
d4fef57c-ca8f-4bfa-bc8f-a2d2412ea20a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,Posterior wall myocardial infarction (PWMI),False,Posterior wall myocardial infarction (PWMI),,,,
7a550b83-211e-416f-aa5d-884398c38b31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
7a550b83-211e-416f-aa5d-884398c38b31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
7a550b83-211e-416f-aa5d-884398c38b31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
7a550b83-211e-416f-aa5d-884398c38b31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
7a550b83-211e-416f-aa5d-884398c38b31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
87498b54-2e64-4035-8d28-0c3051a459a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"The location of the infarction, leads showing ST elevation and depression, and the involved coronary artery are summarized in table 7.1.",True,Posterior wall myocardial infarction (PWMI),,,,
d6f130e7-8b57-413a-82ad-f4c3bc64432f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"Table 7.1: Location of the infarction, leads showing ST elevation and depression, and the involved coronary artery.",True,Posterior wall myocardial infarction (PWMI),,,,
31465fc4-c8ca-4c28-a09e-e35b660d3a24,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,Text,False,Text,,,,
19ac3fb9-a18e-4e20-8153-9d382a61bd4d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"Rhee, June-Wha, Sabatine, Marc S., and Leonard S. Lilly. “Ischemic Heart Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e, edited by Leonard S. Lilly, Chapter 6. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
0d31a3ab-2b34-4c7d-bc65-1e3cc2bb78f2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"Rhee, June-Wha, Sabatine, Marc S., and Leonard S. Lilly. “Acute Coronary Syndromes.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e, edited by Leonard S. Lilly, Chapter 7. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
00b3cd7b-7593-4c6c-91eb-92a1e6a373ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"Surawicz, Borys, Rory Childers, Barbara J. Deal, and Leonard S. Gettes. “AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram.” Circulation 119, no. 10 (2009): e235–e240.",True,Text,,,,
fa99b222-4a12-4fbf-9880-1b02c47c4585,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/#chapter-42-section-1,"Surawicz, Borys, and Timothy Knilans. Chou’s Electrocardiography in Practice, 6th ed. Philadelphia: Saunders, 2008.",True,Text,,,,
3f443258-9519-4cf3-929a-ff2c29a80ba1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,Text,Figure 7.1,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
3f443258-9519-4cf3-929a-ff2c29a80ba1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,Text,Figure 7.1,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
3f443258-9519-4cf3-929a-ff2c29a80ba1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,Text,Figure 7.1,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
3f443258-9519-4cf3-929a-ff2c29a80ba1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,Text,Figure 7.1,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
3f443258-9519-4cf3-929a-ff2c29a80ba1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The process by which atherosclerotic plaques form is summarized in figure 7.1, but there are four fundamental stages:",True,Text,Figure 7.1,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.1-1-scaled.jpg,Figure 7.1: Sequences in progression of atherosclerosis.
803bbd9a-931a-4895-838b-d92ff58008c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,Types of Myocardial Ischemia and Infarction,False,Types of Myocardial Ischemia and Infarction,,,,
1174a188-a235-43b7-a4b9-4776da80a379,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The degree of occlusion caused by the plaque and the oxygen demand of the myocardium determine the degree of ischemia that can develop. Arterial occlusion tends not to be a significant factor until the lumen is occluded by about 70 percent. Vascular occlusion may also be masked by formation of anastomoses (new vessels that bypass the occlusion). Rupture of the plaque and formation of a thrombus can drastically and quickly reduce the lumen and blood flow. The degree and duration of ischemia determine the type of acute coronary syndrome that occurs and the clinical impact. Mild or brief ischemia can lead to angina pectoris with no permanent tissue damage, but when ischemia is prolonged then myocardial infarction becomes more likely, and significant changes in ECG and release of cardiac enzymes are seen.",True,Types of Myocardial Ischemia and Infarction,,,,
f45582ca-d641-4a61-9caf-7d359c5c5467,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,Stable and unstable angina pectoris,False,Stable and unstable angina pectoris,,,,
4ac6e385-b743-40ac-8787-afa6a6bf7110,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"While not considered an acute coronary syndrome, stable angina is pain associated with periods of myocardial ischemia, usually associated with exertion and an increase in myocardial oxygen demand that is unmeet because of insufficient tissue perfusion. The inadequate perfusion is most commonly caused by coronary artery disease (vessel occlusion). Stable angina is predictable and regular, and resolves when the myocardial oxygen demand is reduced (i.e., cessation of exercise).",True,Stable and unstable angina pectoris,,,,
545dda36-996b-4408-a235-1d82178d1a44,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"Unstable angina is more serious and may be an unpredictable exacerbation of anginal pain that had previously been stable. It may occur at rest or lower than usual levels of exertion. Unstable angina is part of the acute coronary syndrome spectrum and may reflect rupture of a plaque that has led to thrombosis. The ECG in unstable angina may show hyperacute T-waves, flattening of the T-waves, inverted T-waves, and ST depression. Without the presence of myocardial damage, unstable angina is not associated with elevated cardiac enzymes (e.g., troponin). Continued or worsening stenosis of the coronary artery leads to tissue infarction and more clinically significant elements of acute coronary syndrome.",True,Stable and unstable angina pectoris,,,,
70c8fc6a-8c6d-47ab-981e-a0cc94d2101a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,Non-ST segment elevation myocardial infarction,False,Non-ST segment elevation myocardial infarction,,,,
48e901ff-92c8-4bf7-96fa-11ee6524e130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
48e901ff-92c8-4bf7-96fa-11ee6524e130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
48e901ff-92c8-4bf7-96fa-11ee6524e130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
48e901ff-92c8-4bf7-96fa-11ee6524e130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
48e901ff-92c8-4bf7-96fa-11ee6524e130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"With non-ST segment elevation myocardial infarction (NSTEMI), there is necrosis of the myocardium. Although, as the name suggests, there is no consistent ST segment elevation in a NSTEMI, other ECG changes may be seen. These include transient ST elevation, ST depression, or new T-wave inversions. The lysing myocytes release their contents including enzymes that can be used as biomarkers of the necrotic event. Presence of elevated cardiac enzymes distinguishes NSTEMI from unstable angina, but denotes myocardial damage and a poorer prognosis. There are several cardiac enzymes that can be detected (myoglobin, creatine kinase, and troponin I), and each has a different timeline from onset of infarction (figure 7.3). But because of improvements in test sensitivity, the test enzyme of choice is troponin I.",True,Non-ST segment elevation myocardial infarction,Figure 7.3,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.3-1-scaled.jpg,Figure 7.3: Timeline of cardiac biomarkers after a myocardial infarction.
ccffcaa6-a9b0-478a-b17b-b42ec63e9053,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,Troponin,False,Troponin,,,,
c5f99931-e0b4-483a-bbf4-c3689b44854c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"Troponin I is a normal protein important in the contractile apparatus of the cardiac myocyte. It is released into the circulation about three to four hours after MI and are still detectable for ten days afterward. The long half-life allows for the late diagnosis of MI but makes it difficult to detect reinfarction (a major complication associated with new thrombus formation during stent placement). Although there are a number causes for troponin elevation unrelated to MI, troponin elevation is much more sensitive and specific than myoglobin and even creatine kinase.",True,Troponin,,,,
1421a57d-54b5-4fb9-b61a-9989ba7e5c9c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,ST segment elevation myocardial infarction,False,ST segment elevation myocardial infarction,,,,
be9afe00-ca3b-4281-a961-0c9e0cd2754a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"ST segment elevation myocardial infarction (STEMI) most often results from complete occlusion of a major epicardial vessel. The resultant myocardial infarction raises cardiac enzymes measured in the blood (as with NSTEMI), but is accompanied by an ST segment elevation on the 12-lead ECG. This is the most serious of the acute coronary syndromes.",True,ST segment elevation myocardial infarction,,,,
84de5ad1-5a03-4343-a8a7-c5d326db494f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,Pathophysiology of a STEMI,False,Pathophysiology of a STEMI,,,,
8e4aa6b5-6a7f-4f68-b517-df9432af316f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The most common cause of a STEMI is rupture of an atherosclerotic plaque. The continued degradation and calcification of the fibrous cap results in it breaking and spilling its contents into the bloodstream. Tissue factor within the necrotic core instigates the coagulation cascade when it is exposed to the blood and a thrombus is formed and the vessel is occluded. Plaques rupture most frequently at their “shoulder,” the thin peripheral edges where proteolytic and apoptotic activity are highest and mechanical forces are most effective. The tissue downstream from the occlusion experiences ischemia and then infarcts. The impact on cardiac function and output depends on the site and extent of the infarcted tissue. For example, if a significant section of the left ventricular wall is involved, then the fall in cardiac output may be catastrophic, or if the papillary muscles of a valve are included, the valve may become incompetent and allow regurgitation.",True,Pathophysiology of a STEMI,,,,
1fb0b703-7071-43ec-985a-ea75eb3f39b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,Physical Exam of a STEMI,False,Physical Exam of a STEMI,,,,
e66ecf09-3b16-46e9-a6da-07cc1094aad2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
e66ecf09-3b16-46e9-a6da-07cc1094aad2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
e66ecf09-3b16-46e9-a6da-07cc1094aad2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
e66ecf09-3b16-46e9-a6da-07cc1094aad2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
e66ecf09-3b16-46e9-a6da-07cc1094aad2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The physical examination findings may include elevated heart rate and blood pressure due to increased sympathetic tone. However, if cardiac function is severely impacted because of the size or location of the infarction, cardiogenic shock may result with a fall in blood pressure. The insufficient ATP production in the ischemic region means the interaction of actin and myosin in the cardiac myocytes cannot be broken and the muscle cannot relax. An S4 heart sound (figure 7.4) occurs when the noncompliant, stiffened left ventricle vibrates when blood enters from the atrium. The S4 sound is also known as an atrial gallop—not because the sound comes from the ventricle, but because it is associated with atrial contraction (and ventricular filling). If the infarction involves an impact of the papillary muscle function, the associated valve will fail and the regurgitation will cause a holosystolic murmur. A STEMI in the left ventricle sufficient to cause congestion and a rise in left-ventricular and end-diastolic pressure can lead to rises in left atrial and pulmonary pressure; this may be heard on the lung exam as rales due to the transient pulmonary edema.",True,Physical Exam of a STEMI,Figure 7.4,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
db5de8b0-058f-4638-b29b-8929344c90e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,Diagnosis of a STEMI,False,Diagnosis of a STEMI,,,,
3c67be66-dc4b-434c-b767-14787cfa291d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
3c67be66-dc4b-434c-b767-14787cfa291d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
3c67be66-dc4b-434c-b767-14787cfa291d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
3c67be66-dc4b-434c-b767-14787cfa291d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
3c67be66-dc4b-434c-b767-14787cfa291d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"As mentioned above the two most important tools for diagnosing a STEMI are the ECG and the presence of cardiac enzymes that have been released into the bloodstream. Figure 7.4 shows the time line of myoglobin, creatine kinase, and troponin elevations after an infarction. Using the values of all three enzymes allowed the history of an infarction to be generated, but amazing improvements in the sensitivity of the troponin I test have allowed it to become the gold standard because of its specificity to the myocardium.",True,Diagnosis of a STEMI,Figure 7.4,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.4-scaled.jpg,Figure 7.4: Comparison of audible and inaudible S4 sounds.
0418406b-6de7-4fba-91c3-f89ca07296c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,Changes in ECG,False,Changes in ECG,,,,
b07ccf3b-8d00-4d34-8b2d-1c85e3d97fde,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
b07ccf3b-8d00-4d34-8b2d-1c85e3d97fde,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
b07ccf3b-8d00-4d34-8b2d-1c85e3d97fde,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
b07ccf3b-8d00-4d34-8b2d-1c85e3d97fde,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
b07ccf3b-8d00-4d34-8b2d-1c85e3d97fde,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The first ECG sign to arise during a STEMI are “hyperacute T-waves” (figure 7.5). These T-waves are taller than normal and caused by the release of intracellular potassium from lysing cells and the consequent hyperkalemia in the surrounding tissue. Hyperacute T-waves are not often seen clinically because they occur so early in the event and prior to the patient’s arrival in the hospital. Subsequent ECG stages are more commonly observed, and these include the ST elevation.",True,Changes in ECG,Figure 7.5,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.5.jpeg,Figure 7.5: Hyperacute T-waves associated with an early myocardial infarction.
4419602d-e4e8-45eb-bc25-8823466f8de7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
4419602d-e4e8-45eb-bc25-8823466f8de7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
4419602d-e4e8-45eb-bc25-8823466f8de7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
4419602d-e4e8-45eb-bc25-8823466f8de7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
4419602d-e4e8-45eb-bc25-8823466f8de7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,Determining which ECG leads show the ST elevation allow for the location of the infarcted tissue to be determined and provide insight into which coronary vessel is effected. How the leads of a twelve-lead ECG relate to the coronary vessels is summarized in figure 7.6. The following looks at the characteristic ECG changes in relation to location in a bit more detail (tip: relate back to figure 7.6 as you read the next sections).,True,Changes in ECG,Figure 7.6,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.6-1-scaled.jpg,"Figure 7.6: Which leads look at which coronary vessels? LCx = left circumflex, LAD = left anterior descending, RCA = right coronary artery."
d624406a-3845-4ef3-918f-fd5ec1914681,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,Anterior wall myocardial infarctions (AWMI),False,Anterior wall myocardial infarctions (AWMI),,,,
83c85a1b-d4e3-4ed0-9764-95c58784f02c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
83c85a1b-d4e3-4ed0-9764-95c58784f02c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
83c85a1b-d4e3-4ed0-9764-95c58784f02c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
83c85a1b-d4e3-4ed0-9764-95c58784f02c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
83c85a1b-d4e3-4ed0-9764-95c58784f02c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The anterior wall is affected when the left anterior descending coronary artery becomes occluded. Additional involvement of lateral and septal regions is indicative of the left main coronary artery being involved. Inclusion of these regions is termed an extensive anterior infarction. The ECG shows ST segment elevation in leads V3 and V4 (the anterior leads), seen as a raised J-point (see figure 7.7). A reciprocal ST depression will be seen in leads II, III, and aVF (the inferior leads). If the extent of the infarction is large, the elevated ST segment may been seen in the lateral and septal leads. The elevated ST segment is also associated in a change in shape of the T-wave as it becomes broader and loses its concave shape on the downward section. This broad T-wave can be higher as well as the ST elevation progresses, and its height can surpass the R-wave. These morphological changes result in a T-wave that looks like a tombstone (see figure 7.7).",True,Anterior wall myocardial infarctions (AWMI),Figure 7.7,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.7-scaled.jpg,Figure 7.7: An ECG showing an anterior wall infarction with the characteristic “tombstoning” of the T-wave.
eab23c9f-37bc-41e1-a514-5d06bc08e3fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,Inferior wall myocardial infarction (IWMI),False,Inferior wall myocardial infarction (IWMI),,,,
82549fe6-9c3a-406d-ac1f-ca8cdb3ccd51,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
82549fe6-9c3a-406d-ac1f-ca8cdb3ccd51,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
82549fe6-9c3a-406d-ac1f-ca8cdb3ccd51,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
82549fe6-9c3a-406d-ac1f-ca8cdb3ccd51,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
82549fe6-9c3a-406d-ac1f-ca8cdb3ccd51,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"Occlusion of the right coronary artery is the usual culprit for an inferior wall myocardial infarction (IWMI), which may be severe enough to extend to posterior regions.  The ECG findings of an acute inferior myocardial infarction (figure 7.9) will be an ST segment elevation in leads II, III, and aVF (the inferior leads) and reciprocal depression in lead aVL (a lateral lead); without the reciprocal depression in aVL, alternative causes of ST segment elevation in the inferior leads should be considered (e.g., pericarditis). Because the right coronary artery perfuses the SA node, bradycardia may occur. An inferior MI can have multiple potential complications, including cardiogenic shock, atrioventricular block, or ventricular fibrillation, and can be fatal.",True,Inferior wall myocardial infarction (IWMI),Figure 7.9,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.9-scaled.jpg,Figure 7.9: IWMI.
fe8e78a2-32d9-4bc3-b364-8f12a143992c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,Posterior wall myocardial infarction (PWMI),False,Posterior wall myocardial infarction (PWMI),,,,
04a24def-fc29-43cd-8378-a5820be12032,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,Diagnosis of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
04a24def-fc29-43cd-8378-a5820be12032,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,Physical Exam of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
04a24def-fc29-43cd-8378-a5820be12032,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,Pathophysiology of a STEMI,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
04a24def-fc29-43cd-8378-a5820be12032,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,Types of Myocardial Ischemia and Infarction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
04a24def-fc29-43cd-8378-a5820be12032,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"Most posterior myocardial infarctions occur with occlusion of the posterior descending artery (which in most people is a branch of the right coronary artery); because of the shared supply, a posterior infarction is often accompanied by an IWMI. The ECG findings include ST segment elevation in V7–V9 (the posterior leads that are placed on the posterior axillary line, not shown in figure 7.11) and ST depression in V1–V4 (the septal and anterior leads, shown in figure 7.10). If an IWMI is also present then there will be an ST elevation in leads II, III, and aVF (the inferior leads). A twelve-lead ECG showing a posterior wall infarction is shown in figure 7.11.",True,Posterior wall myocardial infarction (PWMI),Figure 7.11,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/7.11-scaled.jpg,Figure 7.11: Posterior wall MI.
9580504e-98e5-4f41-8c91-651198824271,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"The location of the infarction, leads showing ST elevation and depression, and the involved coronary artery are summarized in table 7.1.",True,Posterior wall myocardial infarction (PWMI),,,,
3e93bcba-7f19-4cf4-98ee-7dade5dbdec6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"Table 7.1: Location of the infarction, leads showing ST elevation and depression, and the involved coronary artery.",True,Posterior wall myocardial infarction (PWMI),,,,
742e7d38-c259-4612-ac7d-620d448380ff,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,Text,False,Text,,,,
3eefdab6-c6a1-46a2-ac8c-f4128ac47c7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"Rhee, June-Wha, Sabatine, Marc S., and Leonard S. Lilly. “Ischemic Heart Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e, edited by Leonard S. Lilly, Chapter 6. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
ae5e221d-25a5-45ec-b466-8744a49b6edb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"Rhee, June-Wha, Sabatine, Marc S., and Leonard S. Lilly. “Acute Coronary Syndromes.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e, edited by Leonard S. Lilly, Chapter 7. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
bcb91673-659f-4d91-99c8-5b6cc0d05bc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"Surawicz, Borys, Rory Childers, Barbara J. Deal, and Leonard S. Gettes. “AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram.” Circulation 119, no. 10 (2009): e235–e240.",True,Text,,,,
eb1d7807-47fb-4392-88d9-0768e0577bb1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,7. Ischemic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-7-ischemic-heart-disease/,"Surawicz, Borys, and Timothy Knilans. Chou’s Electrocardiography in Practice, 6th ed. Philadelphia: Saunders, 2008.",True,Text,,,,
70a5d101-5e2a-46e9-a9a1-78aa0dd2d4fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,Embryology,False,Embryology,,,,
9f0f09d4-e613-43c5-b0c4-d88febf2b828,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,The most common atrial septal defects arise from:,False,The most common atrial septal defects arise from:,,,,
ac320655-8631-40bf-a7c4-44003a642f6f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"A patent foramen ovale (20 percent of the population) is not a true ASD as no tissue is missing and the remaining tissue acts as a one-way valve, so a PFO does not have the same pathophysiology as a true ASD. ASDs are common in infants with Down syndrome, as are VSDs.",True,The most common atrial septal defects arise from:,,,,
ff7507ba-bb5b-4c42-b863-bdd165e96c8d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,Pathophysiology,False,Pathophysiology,,,,
0ca2e9a4-4235-43f9-ab0c-905df40a4de4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
0ca2e9a4-4235-43f9-ab0c-905df40a4de4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
0ca2e9a4-4235-43f9-ab0c-905df40a4de4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
0ca2e9a4-4235-43f9-ab0c-905df40a4de4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
0ca2e9a4-4235-43f9-ab0c-905df40a4de4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
0ca2e9a4-4235-43f9-ab0c-905df40a4de4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
0ca2e9a4-4235-43f9-ab0c-905df40a4de4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
0ca2e9a4-4235-43f9-ab0c-905df40a4de4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
0ca2e9a4-4235-43f9-ab0c-905df40a4de4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
199d8a5e-d915-41f5-9d3d-5eea4c8dd85e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,Ventricular Septal Defect (VSD),False,Ventricular Septal Defect (VSD),,,,
2207e1e4-c6bd-4d7f-942d-aba1814d1dac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Most ventricular septal defects arise from membraneous portion of the septum (70 percent), while others form in the muscular portion (20 percent); less frequently they occur near the aortic or AV valves.",True,Ventricular Septal Defect (VSD),,,,
905a0d96-2952-42f9-8fba-fd4f61c9a889,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
905a0d96-2952-42f9-8fba-fd4f61c9a889,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
905a0d96-2952-42f9-8fba-fd4f61c9a889,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
905a0d96-2952-42f9-8fba-fd4f61c9a889,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
905a0d96-2952-42f9-8fba-fd4f61c9a889,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
905a0d96-2952-42f9-8fba-fd4f61c9a889,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
905a0d96-2952-42f9-8fba-fd4f61c9a889,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
905a0d96-2952-42f9-8fba-fd4f61c9a889,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
905a0d96-2952-42f9-8fba-fd4f61c9a889,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
aa70f67a-58aa-47d6-848c-2372e6335b6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
aa70f67a-58aa-47d6-848c-2372e6335b6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
aa70f67a-58aa-47d6-848c-2372e6335b6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
aa70f67a-58aa-47d6-848c-2372e6335b6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
aa70f67a-58aa-47d6-848c-2372e6335b6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
aa70f67a-58aa-47d6-848c-2372e6335b6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
aa70f67a-58aa-47d6-848c-2372e6335b6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
aa70f67a-58aa-47d6-848c-2372e6335b6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
aa70f67a-58aa-47d6-848c-2372e6335b6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
9b0b34e2-c605-4829-b940-b7778129ea5f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,Coarctation of the Aorta,False,Coarctation of the Aorta,,,,
baf51c4b-f19b-4d5a-97c8-2f134e75f7fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
baf51c4b-f19b-4d5a-97c8-2f134e75f7fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
baf51c4b-f19b-4d5a-97c8-2f134e75f7fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
baf51c4b-f19b-4d5a-97c8-2f134e75f7fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
baf51c4b-f19b-4d5a-97c8-2f134e75f7fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
baf51c4b-f19b-4d5a-97c8-2f134e75f7fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
baf51c4b-f19b-4d5a-97c8-2f134e75f7fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
baf51c4b-f19b-4d5a-97c8-2f134e75f7fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
baf51c4b-f19b-4d5a-97c8-2f134e75f7fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
2b7ddeef-3daa-4e16-996a-9128398cd540,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The diminished lumen causes increased afterload on the left ventricle. Vessels branching off the aorta before the coarctation can receive normal blood flow, so the head (carotid) and upper extremities (subclavian) are usually properly perfused whereas branching arteries after the coarctation may be underperfused. Consequently, differential cyanosis is a possible manifestation.",True,Coarctation of the Aorta,,,,
10718bcf-894c-46c4-a78a-b6ea3eb0a184,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,Tetralogy of Fallot (ToF),False,Tetralogy of Fallot (ToF),,,,
7a4760f4-973c-4a6a-8a2b-28a1f5d1c029,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,In Tetralogy of Fallot (ToF) the outflow tract (infundibular) portion of the interventricular septum is displaced. This single defect leads to four defects:,True,Tetralogy of Fallot (ToF),,,,
93e3f0c6-c5f9-413c-b352-7115cb701e96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Other defects can be associated with ToF, but the defects listed above lead this to be the most common form of cyanotic congenital heart disease.",True,Tetralogy of Fallot (ToF),,,,
af60813e-aa12-41db-9727-78873b12e12e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
af60813e-aa12-41db-9727-78873b12e12e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
af60813e-aa12-41db-9727-78873b12e12e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
af60813e-aa12-41db-9727-78873b12e12e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
af60813e-aa12-41db-9727-78873b12e12e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
af60813e-aa12-41db-9727-78873b12e12e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
af60813e-aa12-41db-9727-78873b12e12e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
af60813e-aa12-41db-9727-78873b12e12e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
af60813e-aa12-41db-9727-78873b12e12e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
122179b7-183d-407d-9568-e9c309c64fd0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,Transposition of the Great Arteries,False,Transposition of the Great Arteries,,,,
236b9e5b-579c-4497-81b7-5d66ab40a6f8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Although not completely understood, it is thought that failure of the aortic-pulmonary septum to spiral during development results in the great vessels coming off the wrong ventricles—the aorta exits the right, and the pulmonary artery exits the left. Other theories exist.",True,Transposition of the Great Arteries,,,,
895cbe7b-7f2f-4641-a6fa-539f64d1cd91,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
895cbe7b-7f2f-4641-a6fa-539f64d1cd91,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
895cbe7b-7f2f-4641-a6fa-539f64d1cd91,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
895cbe7b-7f2f-4641-a6fa-539f64d1cd91,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
895cbe7b-7f2f-4641-a6fa-539f64d1cd91,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
895cbe7b-7f2f-4641-a6fa-539f64d1cd91,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
895cbe7b-7f2f-4641-a6fa-539f64d1cd91,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
895cbe7b-7f2f-4641-a6fa-539f64d1cd91,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
895cbe7b-7f2f-4641-a6fa-539f64d1cd91,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
8d03a6dc-6832-47fb-953e-5f9cf307cb01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,Patent Ductus Arteriosus,False,Patent Ductus Arteriosus,,,,
cb3ec1c2-1b92-4d52-a7bf-705e9bf6c4ef,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The ductus arteriosus is part of the fetal circulation allowing blood in the pulmonary artery to bypass the nonfunctional, high resistance lungs and instead traverse into the aorta and systemic circulation. The ductus should close at birth, and failure to do so leaves a patent ductus arteriosus (PDA).",True,Patent Ductus Arteriosus,,,,
d331685f-470c-41e0-978f-1aeb22b0fb60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
d331685f-470c-41e0-978f-1aeb22b0fb60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
d331685f-470c-41e0-978f-1aeb22b0fb60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
d331685f-470c-41e0-978f-1aeb22b0fb60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
d331685f-470c-41e0-978f-1aeb22b0fb60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
d331685f-470c-41e0-978f-1aeb22b0fb60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
d331685f-470c-41e0-978f-1aeb22b0fb60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
d331685f-470c-41e0-978f-1aeb22b0fb60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
d331685f-470c-41e0-978f-1aeb22b0fb60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
e3219b6e-0643-4242-8ce2-be68ebbccf30,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The consequences of this are that a greater volume of blood reenters the pulmonary circulation, the left atria, and the left ventricle. Consequently the compartments of the left heart can eventually fail through volume overload. When the left heart fails, the shunt through the PDA can be reversed, and desaturated blood destined for the pulmonary circulation can end up passing through the PDA to the aorta instead—this reversal later in life is called Eisenmenger syndrome. In Eisenmenger’s the upper extremities receive uncontaminated, saturated blood, as their branching arteries are upstream of the desaturated blood entering the aorta at the PDA. Not so for the lower extremities whose arteries branch after the PDA and so receive low oxygen blood. Hence in Eisenmenger syndrome patients, only the feet are cyanosed.",True,Patent Ductus Arteriosus,,,,
ed277b4c-0a9c-4b8c-bde1-40bf8aeb7a07,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,Atrioventricular Canal,False,Atrioventricular Canal,,,,
c2876a14-af63-464b-bdaf-f313627386d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
c2876a14-af63-464b-bdaf-f313627386d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
c2876a14-af63-464b-bdaf-f313627386d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
c2876a14-af63-464b-bdaf-f313627386d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
c2876a14-af63-464b-bdaf-f313627386d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
c2876a14-af63-464b-bdaf-f313627386d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
c2876a14-af63-464b-bdaf-f313627386d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
c2876a14-af63-464b-bdaf-f313627386d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
c2876a14-af63-464b-bdaf-f313627386d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
974946a0-a10f-48d8-b255-5854625a572b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The malformed valves allow regurgitation, and the unrestricted interventricular communication allow a profound left–right shunt. This leads to volume overload in the pulmonary circulation, and heart failure will be produced if there is no correction. Pulmonary artery hypertension (PAH) and premature development of pulmonary vascular obstructive disease are other common outcomes.",True,Atrioventricular Canal,,,,
38784677-a607-48ec-990d-f6a502eae531,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,Truncus Arteriosus,False,Truncus Arteriosus,,,,
38f7669b-8f52-4a28-859d-6bcf408a76ba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
38f7669b-8f52-4a28-859d-6bcf408a76ba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
38f7669b-8f52-4a28-859d-6bcf408a76ba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
38f7669b-8f52-4a28-859d-6bcf408a76ba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
38f7669b-8f52-4a28-859d-6bcf408a76ba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
38f7669b-8f52-4a28-859d-6bcf408a76ba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
38f7669b-8f52-4a28-859d-6bcf408a76ba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
38f7669b-8f52-4a28-859d-6bcf408a76ba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
38f7669b-8f52-4a28-859d-6bcf408a76ba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
a4208a50-27fd-43a0-abb7-f887dba520fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"The underlying issues with TA are 1) mixing of blood from the left (saturated) and right heart (unsaturated), and 2) the common valve can allow regurgitation. In utero the high pulmonary vascular resistance means most blood exiting the heart goes through the aorta and cardiac output is rarely affected. At birth mild cyanosis can be produced by the mixing of blood from the left and right heart, but as pulmonary vascular resistance remains high in the first few days of life, cardiac output my be maintained. As pulmonary vascular resistance continues to fall in the first few weeks of life, a significant left–right shunt can become established as more left ventricular blood finds it “easier” to ascend up the pulmonary artery. Similar to a VSD, this leads to volume overload in the pulmonary circulation and eventually heart failure. The heart failure has a more rapid onset in TA than VSD if the common valve allows regurgitation. The regurgitation lowers end-diastolic ventricular volumes, so cardiac work to maintain cardiac output increases and promotes myocardial ischemia. Add to this the left–right shunt (as seen in VSD) and heart failure is more likely.",True,Truncus Arteriosus,,,,
20b02455-603c-46f2-9342-31a77b52eaf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,Text,False,Text,,,,
338365cf-229f-462a-a031-98082c43433e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Bhansali, Suneet, and Colin Phoon. Truncus Arteriosis. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK534774/, CC BY 4.0.",True,Text,,,,
995ee375-aece-4390-b26d-9b4c9f312271,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Cunningham, Jonathan W., and David W. Brown. “Congenital Heart Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, edited by Leonard S. Lilly, Chapter 16. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2012.",True,Text,,,,
840aca0a-c487-491a-b695-a8457d2cbc98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Dakkak, Wael, and Tony I. Oliver. Ventricular Septal Defect. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK470330/, CC BY 4.0.",True,Text,,,,
51d7dd59-efef-49b1-b87a-858bd257fe67,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Diaz-Frias, Josua, and Melissa Guillaume. Tetralogy of Fallot. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK513288/, CC BY 4.0.",True,Text,,,,
c7943f22-f9f3-4d59-b486-0d892d7fc01d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Gillam-Krakauer, Maria, and Kunal Mahajan. Patent Ductus Ateriosus. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430758/, CC BY 4.0.",True,Text,,,,
eb6a5536-2fab-49e9-8fea-fb6dfd90ac7e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Law, Mark A., and Vijai  S. Tivakaran. Coarctation of the Aorta. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430913/, CC BY 4.0.",True,Text,,,,
7dab3894-5603-4e66-a595-a4a501477845,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Menillo, Alexandra M., Lawrence S. Lee, and Anthony L. Pearson-Shaver. Atrial Septal Defect. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK535440/, CC BY 4.0.",True,Text,,,,
477bb241-ffa8-4452-b076-05fd90b9111e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Szymanski, Michael W., Sheila M. Moore, Stacy M. Kritzmire, and Amandeep Goyal. Transposition of the Great Arteries. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430758/, CC BY 4.0.",True,Text,,,,
740f1bed-fa6b-4651-a963-90a31353aa51,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Truncus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-8,"Umapathi, Krishna Kishore, and Pradyumna Agasthi. Atrioventricular Canal Defects. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK557511/, CC BY 4.0.",True,Text,,,,
8c276072-efd5-488a-b49e-ef5d62b808ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,Embryology,False,Embryology,,,,
3ca03c45-c23c-4d5b-893d-00c6a2fa8c95,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,The most common atrial septal defects arise from:,False,The most common atrial septal defects arise from:,,,,
39e89da0-fb7a-4df8-a317-b4eebf2e9d0b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"A patent foramen ovale (20 percent of the population) is not a true ASD as no tissue is missing and the remaining tissue acts as a one-way valve, so a PFO does not have the same pathophysiology as a true ASD. ASDs are common in infants with Down syndrome, as are VSDs.",True,The most common atrial septal defects arise from:,,,,
460c7244-f228-4194-81cf-a23cea97f60d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,Pathophysiology,False,Pathophysiology,,,,
cd40537d-e238-418d-bd31-8fda2d198ea7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
cd40537d-e238-418d-bd31-8fda2d198ea7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
cd40537d-e238-418d-bd31-8fda2d198ea7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
cd40537d-e238-418d-bd31-8fda2d198ea7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
cd40537d-e238-418d-bd31-8fda2d198ea7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
cd40537d-e238-418d-bd31-8fda2d198ea7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
cd40537d-e238-418d-bd31-8fda2d198ea7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
cd40537d-e238-418d-bd31-8fda2d198ea7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
cd40537d-e238-418d-bd31-8fda2d198ea7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
9e3d3608-1ceb-4971-ab53-c3e98e56d1a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,Ventricular Septal Defect (VSD),False,Ventricular Septal Defect (VSD),,,,
ada040cc-e02e-4457-915d-e772e1f8eee7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Most ventricular septal defects arise from membraneous portion of the septum (70 percent), while others form in the muscular portion (20 percent); less frequently they occur near the aortic or AV valves.",True,Ventricular Septal Defect (VSD),,,,
1b43a605-eee4-40d3-86a1-54197f29098a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
1b43a605-eee4-40d3-86a1-54197f29098a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
1b43a605-eee4-40d3-86a1-54197f29098a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
1b43a605-eee4-40d3-86a1-54197f29098a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
1b43a605-eee4-40d3-86a1-54197f29098a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
1b43a605-eee4-40d3-86a1-54197f29098a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
1b43a605-eee4-40d3-86a1-54197f29098a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
1b43a605-eee4-40d3-86a1-54197f29098a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
1b43a605-eee4-40d3-86a1-54197f29098a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
6d8648a6-0337-4e31-9925-d72cc900cd03,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
6d8648a6-0337-4e31-9925-d72cc900cd03,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
6d8648a6-0337-4e31-9925-d72cc900cd03,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
6d8648a6-0337-4e31-9925-d72cc900cd03,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
6d8648a6-0337-4e31-9925-d72cc900cd03,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
6d8648a6-0337-4e31-9925-d72cc900cd03,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
6d8648a6-0337-4e31-9925-d72cc900cd03,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
6d8648a6-0337-4e31-9925-d72cc900cd03,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
6d8648a6-0337-4e31-9925-d72cc900cd03,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
5ea6908e-3072-449a-95bd-db8a55208462,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,Coarctation of the Aorta,False,Coarctation of the Aorta,,,,
5d6281a5-d018-480b-b2a9-f6a60a456fc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
5d6281a5-d018-480b-b2a9-f6a60a456fc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
5d6281a5-d018-480b-b2a9-f6a60a456fc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
5d6281a5-d018-480b-b2a9-f6a60a456fc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
5d6281a5-d018-480b-b2a9-f6a60a456fc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
5d6281a5-d018-480b-b2a9-f6a60a456fc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
5d6281a5-d018-480b-b2a9-f6a60a456fc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
5d6281a5-d018-480b-b2a9-f6a60a456fc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
5d6281a5-d018-480b-b2a9-f6a60a456fc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
427c4e11-6bff-4da2-9ba9-1388ad4d39d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The diminished lumen causes increased afterload on the left ventricle. Vessels branching off the aorta before the coarctation can receive normal blood flow, so the head (carotid) and upper extremities (subclavian) are usually properly perfused whereas branching arteries after the coarctation may be underperfused. Consequently, differential cyanosis is a possible manifestation.",True,Coarctation of the Aorta,,,,
ecdb3e8f-a5d7-4a5d-8cf6-5611df97d808,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,Tetralogy of Fallot (ToF),False,Tetralogy of Fallot (ToF),,,,
0a0cc2d2-0076-4bc7-b288-ae473d3b57c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,In Tetralogy of Fallot (ToF) the outflow tract (infundibular) portion of the interventricular septum is displaced. This single defect leads to four defects:,True,Tetralogy of Fallot (ToF),,,,
8f6ff889-509e-43b6-9530-4f812e724dc5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Other defects can be associated with ToF, but the defects listed above lead this to be the most common form of cyanotic congenital heart disease.",True,Tetralogy of Fallot (ToF),,,,
751e529c-88ba-4f1e-956a-b85fb7b04525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
751e529c-88ba-4f1e-956a-b85fb7b04525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
751e529c-88ba-4f1e-956a-b85fb7b04525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
751e529c-88ba-4f1e-956a-b85fb7b04525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
751e529c-88ba-4f1e-956a-b85fb7b04525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
751e529c-88ba-4f1e-956a-b85fb7b04525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
751e529c-88ba-4f1e-956a-b85fb7b04525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
751e529c-88ba-4f1e-956a-b85fb7b04525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
751e529c-88ba-4f1e-956a-b85fb7b04525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
8f7d83a8-fa2f-425b-953f-3bd4dbc9fafa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,Transposition of the Great Arteries,False,Transposition of the Great Arteries,,,,
2f8b0d6a-c134-41a0-b925-21afe8f73139,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Although not completely understood, it is thought that failure of the aortic-pulmonary septum to spiral during development results in the great vessels coming off the wrong ventricles—the aorta exits the right, and the pulmonary artery exits the left. Other theories exist.",True,Transposition of the Great Arteries,,,,
2661eb82-1a21-4720-b8ac-81f88aa936f4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
2661eb82-1a21-4720-b8ac-81f88aa936f4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
2661eb82-1a21-4720-b8ac-81f88aa936f4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
2661eb82-1a21-4720-b8ac-81f88aa936f4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
2661eb82-1a21-4720-b8ac-81f88aa936f4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
2661eb82-1a21-4720-b8ac-81f88aa936f4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
2661eb82-1a21-4720-b8ac-81f88aa936f4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
2661eb82-1a21-4720-b8ac-81f88aa936f4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
2661eb82-1a21-4720-b8ac-81f88aa936f4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
e5fee47d-9198-4888-a31b-3772c68bf93d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,Patent Ductus Arteriosus,False,Patent Ductus Arteriosus,,,,
9953779d-7fa6-471f-9fcd-cc6fc722237d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The ductus arteriosus is part of the fetal circulation allowing blood in the pulmonary artery to bypass the nonfunctional, high resistance lungs and instead traverse into the aorta and systemic circulation. The ductus should close at birth, and failure to do so leaves a patent ductus arteriosus (PDA).",True,Patent Ductus Arteriosus,,,,
31106f29-6de5-4549-9a94-fc25f6acf24a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
31106f29-6de5-4549-9a94-fc25f6acf24a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
31106f29-6de5-4549-9a94-fc25f6acf24a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
31106f29-6de5-4549-9a94-fc25f6acf24a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
31106f29-6de5-4549-9a94-fc25f6acf24a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
31106f29-6de5-4549-9a94-fc25f6acf24a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
31106f29-6de5-4549-9a94-fc25f6acf24a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
31106f29-6de5-4549-9a94-fc25f6acf24a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
31106f29-6de5-4549-9a94-fc25f6acf24a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
c09b1cd2-925b-4503-ad7f-225e29810147,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The consequences of this are that a greater volume of blood reenters the pulmonary circulation, the left atria, and the left ventricle. Consequently the compartments of the left heart can eventually fail through volume overload. When the left heart fails, the shunt through the PDA can be reversed, and desaturated blood destined for the pulmonary circulation can end up passing through the PDA to the aorta instead—this reversal later in life is called Eisenmenger syndrome. In Eisenmenger’s the upper extremities receive uncontaminated, saturated blood, as their branching arteries are upstream of the desaturated blood entering the aorta at the PDA. Not so for the lower extremities whose arteries branch after the PDA and so receive low oxygen blood. Hence in Eisenmenger syndrome patients, only the feet are cyanosed.",True,Patent Ductus Arteriosus,,,,
c67e51cb-f2ef-43fe-82fc-0adab13b713f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,Atrioventricular Canal,False,Atrioventricular Canal,,,,
f917bdd4-15ec-4c72-a226-ade0a0db607a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
f917bdd4-15ec-4c72-a226-ade0a0db607a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
f917bdd4-15ec-4c72-a226-ade0a0db607a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
f917bdd4-15ec-4c72-a226-ade0a0db607a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
f917bdd4-15ec-4c72-a226-ade0a0db607a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
f917bdd4-15ec-4c72-a226-ade0a0db607a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
f917bdd4-15ec-4c72-a226-ade0a0db607a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
f917bdd4-15ec-4c72-a226-ade0a0db607a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
f917bdd4-15ec-4c72-a226-ade0a0db607a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
74b1b041-f196-424a-83ab-d2e3cbfc9829,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The malformed valves allow regurgitation, and the unrestricted interventricular communication allow a profound left–right shunt. This leads to volume overload in the pulmonary circulation, and heart failure will be produced if there is no correction. Pulmonary artery hypertension (PAH) and premature development of pulmonary vascular obstructive disease are other common outcomes.",True,Atrioventricular Canal,,,,
113bc41c-45f2-4727-8839-23ed83db9526,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,Truncus Arteriosus,False,Truncus Arteriosus,,,,
1582eb44-a3b7-4042-9874-06653286f13b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
1582eb44-a3b7-4042-9874-06653286f13b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
1582eb44-a3b7-4042-9874-06653286f13b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
1582eb44-a3b7-4042-9874-06653286f13b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
1582eb44-a3b7-4042-9874-06653286f13b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
1582eb44-a3b7-4042-9874-06653286f13b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
1582eb44-a3b7-4042-9874-06653286f13b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
1582eb44-a3b7-4042-9874-06653286f13b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
1582eb44-a3b7-4042-9874-06653286f13b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
7c67c033-55c1-4471-a196-749cd0fe74e0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"The underlying issues with TA are 1) mixing of blood from the left (saturated) and right heart (unsaturated), and 2) the common valve can allow regurgitation. In utero the high pulmonary vascular resistance means most blood exiting the heart goes through the aorta and cardiac output is rarely affected. At birth mild cyanosis can be produced by the mixing of blood from the left and right heart, but as pulmonary vascular resistance remains high in the first few days of life, cardiac output my be maintained. As pulmonary vascular resistance continues to fall in the first few weeks of life, a significant left–right shunt can become established as more left ventricular blood finds it “easier” to ascend up the pulmonary artery. Similar to a VSD, this leads to volume overload in the pulmonary circulation and eventually heart failure. The heart failure has a more rapid onset in TA than VSD if the common valve allows regurgitation. The regurgitation lowers end-diastolic ventricular volumes, so cardiac work to maintain cardiac output increases and promotes myocardial ischemia. Add to this the left–right shunt (as seen in VSD) and heart failure is more likely.",True,Truncus Arteriosus,,,,
9dbeeaa6-bc8e-43ff-bc58-962c50c1004c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,Text,False,Text,,,,
567e3c5b-bd36-4d5d-a4e0-2295f31f27ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Bhansali, Suneet, and Colin Phoon. Truncus Arteriosis. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK534774/, CC BY 4.0.",True,Text,,,,
0e733abb-f6d0-402c-8223-cf639cb2749e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Cunningham, Jonathan W., and David W. Brown. “Congenital Heart Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, edited by Leonard S. Lilly, Chapter 16. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2012.",True,Text,,,,
211c68c0-b7e5-4fbe-83a3-32add227863d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Dakkak, Wael, and Tony I. Oliver. Ventricular Septal Defect. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK470330/, CC BY 4.0.",True,Text,,,,
4a6ad7ae-1225-4324-9c3a-37333d29a703,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Diaz-Frias, Josua, and Melissa Guillaume. Tetralogy of Fallot. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK513288/, CC BY 4.0.",True,Text,,,,
cad97c18-1e7e-47c0-89bb-210e81bb9c53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Gillam-Krakauer, Maria, and Kunal Mahajan. Patent Ductus Ateriosus. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430758/, CC BY 4.0.",True,Text,,,,
eca17822-041f-42b1-ad20-405f1cd765a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Law, Mark A., and Vijai  S. Tivakaran. Coarctation of the Aorta. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430913/, CC BY 4.0.",True,Text,,,,
f9960125-c580-4d8e-b11b-7403444aac2f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Menillo, Alexandra M., Lawrence S. Lee, and Anthony L. Pearson-Shaver. Atrial Septal Defect. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK535440/, CC BY 4.0.",True,Text,,,,
c73c6449-1dee-4029-be1a-95be81b9c93e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Szymanski, Michael W., Sheila M. Moore, Stacy M. Kritzmire, and Amandeep Goyal. Transposition of the Great Arteries. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430758/, CC BY 4.0.",True,Text,,,,
cce97ce3-1d87-4e86-8fc5-269da64453d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrioventricular Canal,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-7,"Umapathi, Krishna Kishore, and Pradyumna Agasthi. Atrioventricular Canal Defects. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK557511/, CC BY 4.0.",True,Text,,,,
c1fdcc51-58b8-4fbd-891a-6dcabbe5dbdf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,Embryology,False,Embryology,,,,
025c2187-3ea9-4963-9c82-c9539e289bf7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,The most common atrial septal defects arise from:,False,The most common atrial septal defects arise from:,,,,
67912e6f-89fb-4ad9-bebe-7eacfae67925,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"A patent foramen ovale (20 percent of the population) is not a true ASD as no tissue is missing and the remaining tissue acts as a one-way valve, so a PFO does not have the same pathophysiology as a true ASD. ASDs are common in infants with Down syndrome, as are VSDs.",True,The most common atrial septal defects arise from:,,,,
0b809450-f527-46be-97fd-565a4e49d871,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,Pathophysiology,False,Pathophysiology,,,,
a8997f69-1ada-43de-b1af-92689970aca6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
a8997f69-1ada-43de-b1af-92689970aca6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
a8997f69-1ada-43de-b1af-92689970aca6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
a8997f69-1ada-43de-b1af-92689970aca6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
a8997f69-1ada-43de-b1af-92689970aca6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
a8997f69-1ada-43de-b1af-92689970aca6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
a8997f69-1ada-43de-b1af-92689970aca6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
a8997f69-1ada-43de-b1af-92689970aca6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
a8997f69-1ada-43de-b1af-92689970aca6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
f6d0548d-b3f8-4f7c-a58b-724d41bb768c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,Ventricular Septal Defect (VSD),False,Ventricular Septal Defect (VSD),,,,
eef6eeed-29a9-47b1-bf13-3d764b24df09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Most ventricular septal defects arise from membraneous portion of the septum (70 percent), while others form in the muscular portion (20 percent); less frequently they occur near the aortic or AV valves.",True,Ventricular Septal Defect (VSD),,,,
c4e63262-3b18-47fd-9134-1585b49eac98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
c4e63262-3b18-47fd-9134-1585b49eac98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
c4e63262-3b18-47fd-9134-1585b49eac98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
c4e63262-3b18-47fd-9134-1585b49eac98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
c4e63262-3b18-47fd-9134-1585b49eac98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
c4e63262-3b18-47fd-9134-1585b49eac98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
c4e63262-3b18-47fd-9134-1585b49eac98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
c4e63262-3b18-47fd-9134-1585b49eac98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
c4e63262-3b18-47fd-9134-1585b49eac98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
a9fc64b1-6c2e-4bb4-bb67-4c6db89782d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
a9fc64b1-6c2e-4bb4-bb67-4c6db89782d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
a9fc64b1-6c2e-4bb4-bb67-4c6db89782d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
a9fc64b1-6c2e-4bb4-bb67-4c6db89782d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
a9fc64b1-6c2e-4bb4-bb67-4c6db89782d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
a9fc64b1-6c2e-4bb4-bb67-4c6db89782d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
a9fc64b1-6c2e-4bb4-bb67-4c6db89782d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
a9fc64b1-6c2e-4bb4-bb67-4c6db89782d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
a9fc64b1-6c2e-4bb4-bb67-4c6db89782d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
d0a0dc34-70bb-4c31-8976-9c47a6f2571b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,Coarctation of the Aorta,False,Coarctation of the Aorta,,,,
4212ffbc-6f29-4c64-93fc-7ea3d351c166,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
4212ffbc-6f29-4c64-93fc-7ea3d351c166,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
4212ffbc-6f29-4c64-93fc-7ea3d351c166,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
4212ffbc-6f29-4c64-93fc-7ea3d351c166,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
4212ffbc-6f29-4c64-93fc-7ea3d351c166,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
4212ffbc-6f29-4c64-93fc-7ea3d351c166,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
4212ffbc-6f29-4c64-93fc-7ea3d351c166,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
4212ffbc-6f29-4c64-93fc-7ea3d351c166,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
4212ffbc-6f29-4c64-93fc-7ea3d351c166,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
43190d1e-0acd-4672-aea2-59c8b90163a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The diminished lumen causes increased afterload on the left ventricle. Vessels branching off the aorta before the coarctation can receive normal blood flow, so the head (carotid) and upper extremities (subclavian) are usually properly perfused whereas branching arteries after the coarctation may be underperfused. Consequently, differential cyanosis is a possible manifestation.",True,Coarctation of the Aorta,,,,
4f070b3f-2279-444c-93bd-0498d4e27dfd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,Tetralogy of Fallot (ToF),False,Tetralogy of Fallot (ToF),,,,
e06fe9a0-4656-461a-8c29-cf8add8667d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,In Tetralogy of Fallot (ToF) the outflow tract (infundibular) portion of the interventricular septum is displaced. This single defect leads to four defects:,True,Tetralogy of Fallot (ToF),,,,
2288a17f-f9e0-40bc-9a9f-a9e7e9871cd0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Other defects can be associated with ToF, but the defects listed above lead this to be the most common form of cyanotic congenital heart disease.",True,Tetralogy of Fallot (ToF),,,,
73a08149-ff55-410a-a61a-1abb3e81315b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
73a08149-ff55-410a-a61a-1abb3e81315b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
73a08149-ff55-410a-a61a-1abb3e81315b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
73a08149-ff55-410a-a61a-1abb3e81315b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
73a08149-ff55-410a-a61a-1abb3e81315b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
73a08149-ff55-410a-a61a-1abb3e81315b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
73a08149-ff55-410a-a61a-1abb3e81315b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
73a08149-ff55-410a-a61a-1abb3e81315b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
73a08149-ff55-410a-a61a-1abb3e81315b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
b258f2cc-852a-4d08-a70e-22c1a1468069,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,Transposition of the Great Arteries,False,Transposition of the Great Arteries,,,,
e4998a0c-6cbd-4097-bc60-01a8bfde8c81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Although not completely understood, it is thought that failure of the aortic-pulmonary septum to spiral during development results in the great vessels coming off the wrong ventricles—the aorta exits the right, and the pulmonary artery exits the left. Other theories exist.",True,Transposition of the Great Arteries,,,,
4d2ed45d-cfef-456f-a3d9-5edea0fc2fd7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
4d2ed45d-cfef-456f-a3d9-5edea0fc2fd7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
4d2ed45d-cfef-456f-a3d9-5edea0fc2fd7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
4d2ed45d-cfef-456f-a3d9-5edea0fc2fd7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
4d2ed45d-cfef-456f-a3d9-5edea0fc2fd7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
4d2ed45d-cfef-456f-a3d9-5edea0fc2fd7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
4d2ed45d-cfef-456f-a3d9-5edea0fc2fd7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
4d2ed45d-cfef-456f-a3d9-5edea0fc2fd7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
4d2ed45d-cfef-456f-a3d9-5edea0fc2fd7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
e5745788-855e-4464-a2e4-b497fafd1031,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,Patent Ductus Arteriosus,False,Patent Ductus Arteriosus,,,,
d87bb4ba-3a06-45d5-b773-65e93c0d5d7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The ductus arteriosus is part of the fetal circulation allowing blood in the pulmonary artery to bypass the nonfunctional, high resistance lungs and instead traverse into the aorta and systemic circulation. The ductus should close at birth, and failure to do so leaves a patent ductus arteriosus (PDA).",True,Patent Ductus Arteriosus,,,,
da8981d4-b50f-46d3-8794-f3355dd04eec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
da8981d4-b50f-46d3-8794-f3355dd04eec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
da8981d4-b50f-46d3-8794-f3355dd04eec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
da8981d4-b50f-46d3-8794-f3355dd04eec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
da8981d4-b50f-46d3-8794-f3355dd04eec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
da8981d4-b50f-46d3-8794-f3355dd04eec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
da8981d4-b50f-46d3-8794-f3355dd04eec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
da8981d4-b50f-46d3-8794-f3355dd04eec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
da8981d4-b50f-46d3-8794-f3355dd04eec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
46e19a38-2e5d-4e06-8ff0-f82ded47c6c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The consequences of this are that a greater volume of blood reenters the pulmonary circulation, the left atria, and the left ventricle. Consequently the compartments of the left heart can eventually fail through volume overload. When the left heart fails, the shunt through the PDA can be reversed, and desaturated blood destined for the pulmonary circulation can end up passing through the PDA to the aorta instead—this reversal later in life is called Eisenmenger syndrome. In Eisenmenger’s the upper extremities receive uncontaminated, saturated blood, as their branching arteries are upstream of the desaturated blood entering the aorta at the PDA. Not so for the lower extremities whose arteries branch after the PDA and so receive low oxygen blood. Hence in Eisenmenger syndrome patients, only the feet are cyanosed.",True,Patent Ductus Arteriosus,,,,
1fab2391-526f-400e-8f67-7623195ceafd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,Atrioventricular Canal,False,Atrioventricular Canal,,,,
a68eff9a-ab33-4bdd-a7d6-e19054080920,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
a68eff9a-ab33-4bdd-a7d6-e19054080920,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
a68eff9a-ab33-4bdd-a7d6-e19054080920,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
a68eff9a-ab33-4bdd-a7d6-e19054080920,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
a68eff9a-ab33-4bdd-a7d6-e19054080920,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
a68eff9a-ab33-4bdd-a7d6-e19054080920,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
a68eff9a-ab33-4bdd-a7d6-e19054080920,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
a68eff9a-ab33-4bdd-a7d6-e19054080920,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
a68eff9a-ab33-4bdd-a7d6-e19054080920,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
b394a054-167b-4404-a9b0-fcaa244bdf61,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The malformed valves allow regurgitation, and the unrestricted interventricular communication allow a profound left–right shunt. This leads to volume overload in the pulmonary circulation, and heart failure will be produced if there is no correction. Pulmonary artery hypertension (PAH) and premature development of pulmonary vascular obstructive disease are other common outcomes.",True,Atrioventricular Canal,,,,
926502d7-5e33-4138-9ac2-07b7f882c1fd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,Truncus Arteriosus,False,Truncus Arteriosus,,,,
50bc8ef9-3178-48cd-bc16-ad9e3a0072a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
50bc8ef9-3178-48cd-bc16-ad9e3a0072a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
50bc8ef9-3178-48cd-bc16-ad9e3a0072a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
50bc8ef9-3178-48cd-bc16-ad9e3a0072a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
50bc8ef9-3178-48cd-bc16-ad9e3a0072a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
50bc8ef9-3178-48cd-bc16-ad9e3a0072a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
50bc8ef9-3178-48cd-bc16-ad9e3a0072a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
50bc8ef9-3178-48cd-bc16-ad9e3a0072a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
50bc8ef9-3178-48cd-bc16-ad9e3a0072a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
b8720960-5aa8-4bbe-bab6-0626c6f259ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"The underlying issues with TA are 1) mixing of blood from the left (saturated) and right heart (unsaturated), and 2) the common valve can allow regurgitation. In utero the high pulmonary vascular resistance means most blood exiting the heart goes through the aorta and cardiac output is rarely affected. At birth mild cyanosis can be produced by the mixing of blood from the left and right heart, but as pulmonary vascular resistance remains high in the first few days of life, cardiac output my be maintained. As pulmonary vascular resistance continues to fall in the first few weeks of life, a significant left–right shunt can become established as more left ventricular blood finds it “easier” to ascend up the pulmonary artery. Similar to a VSD, this leads to volume overload in the pulmonary circulation and eventually heart failure. The heart failure has a more rapid onset in TA than VSD if the common valve allows regurgitation. The regurgitation lowers end-diastolic ventricular volumes, so cardiac work to maintain cardiac output increases and promotes myocardial ischemia. Add to this the left–right shunt (as seen in VSD) and heart failure is more likely.",True,Truncus Arteriosus,,,,
5b634f47-edfc-4102-a9f7-f5d5280811f4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,Text,False,Text,,,,
db7eee11-4899-44a9-a498-de79f6a0b924,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Bhansali, Suneet, and Colin Phoon. Truncus Arteriosis. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK534774/, CC BY 4.0.",True,Text,,,,
2247994a-eac5-4b97-ac12-1f87aa061ddd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Cunningham, Jonathan W., and David W. Brown. “Congenital Heart Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, edited by Leonard S. Lilly, Chapter 16. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2012.",True,Text,,,,
1a4ad96e-899a-4e0c-9b17-be882afb968d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Dakkak, Wael, and Tony I. Oliver. Ventricular Septal Defect. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK470330/, CC BY 4.0.",True,Text,,,,
8f2c98a8-29b6-4210-9c21-4c267443901e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Diaz-Frias, Josua, and Melissa Guillaume. Tetralogy of Fallot. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK513288/, CC BY 4.0.",True,Text,,,,
d3404734-1175-4f35-8a52-998bd5332b59,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Gillam-Krakauer, Maria, and Kunal Mahajan. Patent Ductus Ateriosus. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430758/, CC BY 4.0.",True,Text,,,,
ab809f2b-b2af-410c-a671-89176f6a8f88,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Law, Mark A., and Vijai  S. Tivakaran. Coarctation of the Aorta. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430913/, CC BY 4.0.",True,Text,,,,
0b68df53-0a68-46bb-a9ff-cd3d601c7781,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Menillo, Alexandra M., Lawrence S. Lee, and Anthony L. Pearson-Shaver. Atrial Septal Defect. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK535440/, CC BY 4.0.",True,Text,,,,
a9767998-16b9-4f13-b5c1-ed5ed6e614cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Szymanski, Michael W., Sheila M. Moore, Stacy M. Kritzmire, and Amandeep Goyal. Transposition of the Great Arteries. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430758/, CC BY 4.0.",True,Text,,,,
b0df6cec-b0c5-409b-8cd1-6c0ed3b1b612,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-6,"Umapathi, Krishna Kishore, and Pradyumna Agasthi. Atrioventricular Canal Defects. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK557511/, CC BY 4.0.",True,Text,,,,
a010a4c1-5d54-4aa9-a642-93dd92632925,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,Embryology,False,Embryology,,,,
df57424b-b787-4982-af09-a853331be057,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,The most common atrial septal defects arise from:,False,The most common atrial septal defects arise from:,,,,
111c7303-1b9b-4094-be4e-ab0469fca7f8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"A patent foramen ovale (20 percent of the population) is not a true ASD as no tissue is missing and the remaining tissue acts as a one-way valve, so a PFO does not have the same pathophysiology as a true ASD. ASDs are common in infants with Down syndrome, as are VSDs.",True,The most common atrial septal defects arise from:,,,,
94ab44b4-d77d-491e-9482-7c79d2bdb8f3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,Pathophysiology,False,Pathophysiology,,,,
4beb28e1-b696-43b8-952b-d80550835cb5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
4beb28e1-b696-43b8-952b-d80550835cb5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
4beb28e1-b696-43b8-952b-d80550835cb5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
4beb28e1-b696-43b8-952b-d80550835cb5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
4beb28e1-b696-43b8-952b-d80550835cb5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
4beb28e1-b696-43b8-952b-d80550835cb5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
4beb28e1-b696-43b8-952b-d80550835cb5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
4beb28e1-b696-43b8-952b-d80550835cb5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
4beb28e1-b696-43b8-952b-d80550835cb5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
b8f1e8ca-528c-4ffd-90de-12ffb8fd9518,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,Ventricular Septal Defect (VSD),False,Ventricular Septal Defect (VSD),,,,
33c6c2e8-0604-42c0-9dfd-9cf6df278bf2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Most ventricular septal defects arise from membraneous portion of the septum (70 percent), while others form in the muscular portion (20 percent); less frequently they occur near the aortic or AV valves.",True,Ventricular Septal Defect (VSD),,,,
e26493ba-8f2d-4d32-8d63-6c4cd48db885,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
e26493ba-8f2d-4d32-8d63-6c4cd48db885,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
e26493ba-8f2d-4d32-8d63-6c4cd48db885,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
e26493ba-8f2d-4d32-8d63-6c4cd48db885,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
e26493ba-8f2d-4d32-8d63-6c4cd48db885,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
e26493ba-8f2d-4d32-8d63-6c4cd48db885,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
e26493ba-8f2d-4d32-8d63-6c4cd48db885,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
e26493ba-8f2d-4d32-8d63-6c4cd48db885,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
e26493ba-8f2d-4d32-8d63-6c4cd48db885,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
b03b7f2d-99a6-4a8f-b6f1-dec5a7502e30,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
b03b7f2d-99a6-4a8f-b6f1-dec5a7502e30,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
b03b7f2d-99a6-4a8f-b6f1-dec5a7502e30,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
b03b7f2d-99a6-4a8f-b6f1-dec5a7502e30,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
b03b7f2d-99a6-4a8f-b6f1-dec5a7502e30,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
b03b7f2d-99a6-4a8f-b6f1-dec5a7502e30,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
b03b7f2d-99a6-4a8f-b6f1-dec5a7502e30,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
b03b7f2d-99a6-4a8f-b6f1-dec5a7502e30,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
b03b7f2d-99a6-4a8f-b6f1-dec5a7502e30,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
a1e5b4b9-ede9-4a93-b2fa-564ca0df4ed6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,Coarctation of the Aorta,False,Coarctation of the Aorta,,,,
0e540d98-bbd3-4f37-9d27-05d688811175,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
0e540d98-bbd3-4f37-9d27-05d688811175,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
0e540d98-bbd3-4f37-9d27-05d688811175,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
0e540d98-bbd3-4f37-9d27-05d688811175,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
0e540d98-bbd3-4f37-9d27-05d688811175,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
0e540d98-bbd3-4f37-9d27-05d688811175,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
0e540d98-bbd3-4f37-9d27-05d688811175,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
0e540d98-bbd3-4f37-9d27-05d688811175,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
0e540d98-bbd3-4f37-9d27-05d688811175,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
6ab0d305-ae31-49bd-a422-183dfcb5e37f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The diminished lumen causes increased afterload on the left ventricle. Vessels branching off the aorta before the coarctation can receive normal blood flow, so the head (carotid) and upper extremities (subclavian) are usually properly perfused whereas branching arteries after the coarctation may be underperfused. Consequently, differential cyanosis is a possible manifestation.",True,Coarctation of the Aorta,,,,
f6a88a99-4995-4d56-a9ef-4fa6a2bd7194,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,Tetralogy of Fallot (ToF),False,Tetralogy of Fallot (ToF),,,,
2fb6dd64-1f4e-48b6-b98e-a15013804f93,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,In Tetralogy of Fallot (ToF) the outflow tract (infundibular) portion of the interventricular septum is displaced. This single defect leads to four defects:,True,Tetralogy of Fallot (ToF),,,,
e5562872-8bbe-4ca9-889f-297c205d9492,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Other defects can be associated with ToF, but the defects listed above lead this to be the most common form of cyanotic congenital heart disease.",True,Tetralogy of Fallot (ToF),,,,
0279c1b8-decc-4750-8bb4-8aae98111060,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
0279c1b8-decc-4750-8bb4-8aae98111060,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
0279c1b8-decc-4750-8bb4-8aae98111060,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
0279c1b8-decc-4750-8bb4-8aae98111060,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
0279c1b8-decc-4750-8bb4-8aae98111060,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
0279c1b8-decc-4750-8bb4-8aae98111060,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
0279c1b8-decc-4750-8bb4-8aae98111060,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
0279c1b8-decc-4750-8bb4-8aae98111060,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
0279c1b8-decc-4750-8bb4-8aae98111060,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
bc751334-ac43-48b9-9ac7-da605b395b5b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,Transposition of the Great Arteries,False,Transposition of the Great Arteries,,,,
5206e1b7-ec16-42b0-8660-1a2df9a4d696,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Although not completely understood, it is thought that failure of the aortic-pulmonary septum to spiral during development results in the great vessels coming off the wrong ventricles—the aorta exits the right, and the pulmonary artery exits the left. Other theories exist.",True,Transposition of the Great Arteries,,,,
9ef46688-aa0e-4f1f-99b9-21ca1f2a9f05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
9ef46688-aa0e-4f1f-99b9-21ca1f2a9f05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
9ef46688-aa0e-4f1f-99b9-21ca1f2a9f05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
9ef46688-aa0e-4f1f-99b9-21ca1f2a9f05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
9ef46688-aa0e-4f1f-99b9-21ca1f2a9f05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
9ef46688-aa0e-4f1f-99b9-21ca1f2a9f05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
9ef46688-aa0e-4f1f-99b9-21ca1f2a9f05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
9ef46688-aa0e-4f1f-99b9-21ca1f2a9f05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
9ef46688-aa0e-4f1f-99b9-21ca1f2a9f05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
cb2b146a-7d4f-42f2-8dd9-2473cc172278,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,Patent Ductus Arteriosus,False,Patent Ductus Arteriosus,,,,
32275d74-0e1f-4ded-ba8c-6b291a6fa82e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The ductus arteriosus is part of the fetal circulation allowing blood in the pulmonary artery to bypass the nonfunctional, high resistance lungs and instead traverse into the aorta and systemic circulation. The ductus should close at birth, and failure to do so leaves a patent ductus arteriosus (PDA).",True,Patent Ductus Arteriosus,,,,
f19483c7-fd46-4682-aec6-b52e96484d5b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
f19483c7-fd46-4682-aec6-b52e96484d5b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
f19483c7-fd46-4682-aec6-b52e96484d5b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
f19483c7-fd46-4682-aec6-b52e96484d5b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
f19483c7-fd46-4682-aec6-b52e96484d5b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
f19483c7-fd46-4682-aec6-b52e96484d5b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
f19483c7-fd46-4682-aec6-b52e96484d5b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
f19483c7-fd46-4682-aec6-b52e96484d5b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
f19483c7-fd46-4682-aec6-b52e96484d5b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
74a6cf99-92cc-4271-8382-6b82b362a96c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The consequences of this are that a greater volume of blood reenters the pulmonary circulation, the left atria, and the left ventricle. Consequently the compartments of the left heart can eventually fail through volume overload. When the left heart fails, the shunt through the PDA can be reversed, and desaturated blood destined for the pulmonary circulation can end up passing through the PDA to the aorta instead—this reversal later in life is called Eisenmenger syndrome. In Eisenmenger’s the upper extremities receive uncontaminated, saturated blood, as their branching arteries are upstream of the desaturated blood entering the aorta at the PDA. Not so for the lower extremities whose arteries branch after the PDA and so receive low oxygen blood. Hence in Eisenmenger syndrome patients, only the feet are cyanosed.",True,Patent Ductus Arteriosus,,,,
29d36769-b86c-4912-9973-8c3a0a4c98ba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,Atrioventricular Canal,False,Atrioventricular Canal,,,,
6841b982-1bf3-4766-99ac-4618c8a35909,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
6841b982-1bf3-4766-99ac-4618c8a35909,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
6841b982-1bf3-4766-99ac-4618c8a35909,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
6841b982-1bf3-4766-99ac-4618c8a35909,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
6841b982-1bf3-4766-99ac-4618c8a35909,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
6841b982-1bf3-4766-99ac-4618c8a35909,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
6841b982-1bf3-4766-99ac-4618c8a35909,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
6841b982-1bf3-4766-99ac-4618c8a35909,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
6841b982-1bf3-4766-99ac-4618c8a35909,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
b07a693a-553d-467b-84fb-8d685a4d062a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The malformed valves allow regurgitation, and the unrestricted interventricular communication allow a profound left–right shunt. This leads to volume overload in the pulmonary circulation, and heart failure will be produced if there is no correction. Pulmonary artery hypertension (PAH) and premature development of pulmonary vascular obstructive disease are other common outcomes.",True,Atrioventricular Canal,,,,
5c5efc4a-6812-4732-ab6d-5f0fb83d6025,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,Truncus Arteriosus,False,Truncus Arteriosus,,,,
0bc8be43-aa59-42a7-ba20-66aabcb49ca2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
0bc8be43-aa59-42a7-ba20-66aabcb49ca2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
0bc8be43-aa59-42a7-ba20-66aabcb49ca2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
0bc8be43-aa59-42a7-ba20-66aabcb49ca2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
0bc8be43-aa59-42a7-ba20-66aabcb49ca2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
0bc8be43-aa59-42a7-ba20-66aabcb49ca2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
0bc8be43-aa59-42a7-ba20-66aabcb49ca2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
0bc8be43-aa59-42a7-ba20-66aabcb49ca2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
0bc8be43-aa59-42a7-ba20-66aabcb49ca2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
8fef5c47-d28d-40b1-ba3c-c2799caee7a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"The underlying issues with TA are 1) mixing of blood from the left (saturated) and right heart (unsaturated), and 2) the common valve can allow regurgitation. In utero the high pulmonary vascular resistance means most blood exiting the heart goes through the aorta and cardiac output is rarely affected. At birth mild cyanosis can be produced by the mixing of blood from the left and right heart, but as pulmonary vascular resistance remains high in the first few days of life, cardiac output my be maintained. As pulmonary vascular resistance continues to fall in the first few weeks of life, a significant left–right shunt can become established as more left ventricular blood finds it “easier” to ascend up the pulmonary artery. Similar to a VSD, this leads to volume overload in the pulmonary circulation and eventually heart failure. The heart failure has a more rapid onset in TA than VSD if the common valve allows regurgitation. The regurgitation lowers end-diastolic ventricular volumes, so cardiac work to maintain cardiac output increases and promotes myocardial ischemia. Add to this the left–right shunt (as seen in VSD) and heart failure is more likely.",True,Truncus Arteriosus,,,,
3f8508a4-de55-4558-ae12-8c90aabbe1a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,Text,False,Text,,,,
ef63ddf5-179d-46ea-8060-7634d9a1b2f9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Bhansali, Suneet, and Colin Phoon. Truncus Arteriosis. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK534774/, CC BY 4.0.",True,Text,,,,
c485884a-68c6-4bfc-ae41-b80a48af990c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Cunningham, Jonathan W., and David W. Brown. “Congenital Heart Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, edited by Leonard S. Lilly, Chapter 16. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2012.",True,Text,,,,
0b0ec48b-2ee0-4d25-88ca-53eed9be6ce7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Dakkak, Wael, and Tony I. Oliver. Ventricular Septal Defect. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK470330/, CC BY 4.0.",True,Text,,,,
f6ff93d5-1c5a-435f-ba51-a22a37600e80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Diaz-Frias, Josua, and Melissa Guillaume. Tetralogy of Fallot. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK513288/, CC BY 4.0.",True,Text,,,,
826e3eed-86a5-48f5-87df-5cefadb0759f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Gillam-Krakauer, Maria, and Kunal Mahajan. Patent Ductus Ateriosus. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430758/, CC BY 4.0.",True,Text,,,,
d7c8dd6a-5d7c-46d0-b459-a6aff1312a5a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Law, Mark A., and Vijai  S. Tivakaran. Coarctation of the Aorta. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430913/, CC BY 4.0.",True,Text,,,,
e4831330-9ad0-433a-bc52-c5de1f85eb20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Menillo, Alexandra M., Lawrence S. Lee, and Anthony L. Pearson-Shaver. Atrial Septal Defect. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK535440/, CC BY 4.0.",True,Text,,,,
e2626020-41d9-4657-ad50-3d7e233c30ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Szymanski, Michael W., Sheila M. Moore, Stacy M. Kritzmire, and Amandeep Goyal. Transposition of the Great Arteries. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430758/, CC BY 4.0.",True,Text,,,,
7e0c625c-ca7b-404d-a1c4-fcc1053b7f4a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-5,"Umapathi, Krishna Kishore, and Pradyumna Agasthi. Atrioventricular Canal Defects. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK557511/, CC BY 4.0.",True,Text,,,,
e86e3269-c16b-472a-aacf-c5e7d9389a3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,Embryology,False,Embryology,,,,
38a6fbb9-b5fd-4106-ad34-335d2f64982a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,The most common atrial septal defects arise from:,False,The most common atrial septal defects arise from:,,,,
cf6e9ffa-122e-4ae4-b9cc-626389d596d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"A patent foramen ovale (20 percent of the population) is not a true ASD as no tissue is missing and the remaining tissue acts as a one-way valve, so a PFO does not have the same pathophysiology as a true ASD. ASDs are common in infants with Down syndrome, as are VSDs.",True,The most common atrial septal defects arise from:,,,,
00ca75b7-7697-4215-9b42-df09c699d9b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,Pathophysiology,False,Pathophysiology,,,,
b8a9d198-5922-42a0-8739-114234781f4f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
b8a9d198-5922-42a0-8739-114234781f4f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
b8a9d198-5922-42a0-8739-114234781f4f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
b8a9d198-5922-42a0-8739-114234781f4f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
b8a9d198-5922-42a0-8739-114234781f4f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
b8a9d198-5922-42a0-8739-114234781f4f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
b8a9d198-5922-42a0-8739-114234781f4f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
b8a9d198-5922-42a0-8739-114234781f4f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
b8a9d198-5922-42a0-8739-114234781f4f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
085d3768-3feb-45fd-a776-5580daf88a48,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,Ventricular Septal Defect (VSD),False,Ventricular Septal Defect (VSD),,,,
fe2546bb-feb1-488d-bc7c-2302d39e6673,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Most ventricular septal defects arise from membraneous portion of the septum (70 percent), while others form in the muscular portion (20 percent); less frequently they occur near the aortic or AV valves.",True,Ventricular Septal Defect (VSD),,,,
7ee45e90-64ce-44b7-a5d2-bae11112df84,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
7ee45e90-64ce-44b7-a5d2-bae11112df84,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
7ee45e90-64ce-44b7-a5d2-bae11112df84,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
7ee45e90-64ce-44b7-a5d2-bae11112df84,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
7ee45e90-64ce-44b7-a5d2-bae11112df84,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
7ee45e90-64ce-44b7-a5d2-bae11112df84,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
7ee45e90-64ce-44b7-a5d2-bae11112df84,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
7ee45e90-64ce-44b7-a5d2-bae11112df84,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
7ee45e90-64ce-44b7-a5d2-bae11112df84,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
2871b0bd-c8bf-4a53-8fa6-20004917dfc7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
2871b0bd-c8bf-4a53-8fa6-20004917dfc7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
2871b0bd-c8bf-4a53-8fa6-20004917dfc7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
2871b0bd-c8bf-4a53-8fa6-20004917dfc7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
2871b0bd-c8bf-4a53-8fa6-20004917dfc7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
2871b0bd-c8bf-4a53-8fa6-20004917dfc7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
2871b0bd-c8bf-4a53-8fa6-20004917dfc7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
2871b0bd-c8bf-4a53-8fa6-20004917dfc7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
2871b0bd-c8bf-4a53-8fa6-20004917dfc7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
2b0e744d-4254-4a23-ac89-41aeeb4f1a21,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,Coarctation of the Aorta,False,Coarctation of the Aorta,,,,
a886cbb2-f415-4d68-a962-9d43d4639c68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
a886cbb2-f415-4d68-a962-9d43d4639c68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
a886cbb2-f415-4d68-a962-9d43d4639c68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
a886cbb2-f415-4d68-a962-9d43d4639c68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
a886cbb2-f415-4d68-a962-9d43d4639c68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
a886cbb2-f415-4d68-a962-9d43d4639c68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
a886cbb2-f415-4d68-a962-9d43d4639c68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
a886cbb2-f415-4d68-a962-9d43d4639c68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
a886cbb2-f415-4d68-a962-9d43d4639c68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
1605b44c-2cce-4dc6-9471-9766f562d3e9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The diminished lumen causes increased afterload on the left ventricle. Vessels branching off the aorta before the coarctation can receive normal blood flow, so the head (carotid) and upper extremities (subclavian) are usually properly perfused whereas branching arteries after the coarctation may be underperfused. Consequently, differential cyanosis is a possible manifestation.",True,Coarctation of the Aorta,,,,
8cc294ee-8eec-446d-8840-eed5f87c8972,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,Tetralogy of Fallot (ToF),False,Tetralogy of Fallot (ToF),,,,
b1f17cc5-6dd2-4cc2-ac12-45dd24d17e49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,In Tetralogy of Fallot (ToF) the outflow tract (infundibular) portion of the interventricular septum is displaced. This single defect leads to four defects:,True,Tetralogy of Fallot (ToF),,,,
d1826944-b2ca-40e3-9a31-587baf7aec89,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Other defects can be associated with ToF, but the defects listed above lead this to be the most common form of cyanotic congenital heart disease.",True,Tetralogy of Fallot (ToF),,,,
c0be665f-884e-477d-a3fc-e108cb8b3718,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
c0be665f-884e-477d-a3fc-e108cb8b3718,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
c0be665f-884e-477d-a3fc-e108cb8b3718,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
c0be665f-884e-477d-a3fc-e108cb8b3718,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
c0be665f-884e-477d-a3fc-e108cb8b3718,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
c0be665f-884e-477d-a3fc-e108cb8b3718,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
c0be665f-884e-477d-a3fc-e108cb8b3718,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
c0be665f-884e-477d-a3fc-e108cb8b3718,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
c0be665f-884e-477d-a3fc-e108cb8b3718,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
2940154d-d61a-4d77-bd61-2a39bb906e58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,Transposition of the Great Arteries,False,Transposition of the Great Arteries,,,,
a7a90f10-e555-4ca6-8de9-64ea013bb546,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Although not completely understood, it is thought that failure of the aortic-pulmonary septum to spiral during development results in the great vessels coming off the wrong ventricles—the aorta exits the right, and the pulmonary artery exits the left. Other theories exist.",True,Transposition of the Great Arteries,,,,
d207884b-dcf3-4a3e-adbc-c842f89a4a98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
d207884b-dcf3-4a3e-adbc-c842f89a4a98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
d207884b-dcf3-4a3e-adbc-c842f89a4a98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
d207884b-dcf3-4a3e-adbc-c842f89a4a98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
d207884b-dcf3-4a3e-adbc-c842f89a4a98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
d207884b-dcf3-4a3e-adbc-c842f89a4a98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
d207884b-dcf3-4a3e-adbc-c842f89a4a98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
d207884b-dcf3-4a3e-adbc-c842f89a4a98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
d207884b-dcf3-4a3e-adbc-c842f89a4a98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
b50a3ceb-93fa-4945-97aa-4ea26ff73057,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,Patent Ductus Arteriosus,False,Patent Ductus Arteriosus,,,,
2ca96425-2e83-4a11-81e4-e0698b588974,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The ductus arteriosus is part of the fetal circulation allowing blood in the pulmonary artery to bypass the nonfunctional, high resistance lungs and instead traverse into the aorta and systemic circulation. The ductus should close at birth, and failure to do so leaves a patent ductus arteriosus (PDA).",True,Patent Ductus Arteriosus,,,,
bc0070ad-5c46-448f-bedb-2bcbf821a3f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
bc0070ad-5c46-448f-bedb-2bcbf821a3f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
bc0070ad-5c46-448f-bedb-2bcbf821a3f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
bc0070ad-5c46-448f-bedb-2bcbf821a3f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
bc0070ad-5c46-448f-bedb-2bcbf821a3f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
bc0070ad-5c46-448f-bedb-2bcbf821a3f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
bc0070ad-5c46-448f-bedb-2bcbf821a3f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
bc0070ad-5c46-448f-bedb-2bcbf821a3f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
bc0070ad-5c46-448f-bedb-2bcbf821a3f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
b83a84b8-1874-4839-aca9-b3c9801a1d36,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The consequences of this are that a greater volume of blood reenters the pulmonary circulation, the left atria, and the left ventricle. Consequently the compartments of the left heart can eventually fail through volume overload. When the left heart fails, the shunt through the PDA can be reversed, and desaturated blood destined for the pulmonary circulation can end up passing through the PDA to the aorta instead—this reversal later in life is called Eisenmenger syndrome. In Eisenmenger’s the upper extremities receive uncontaminated, saturated blood, as their branching arteries are upstream of the desaturated blood entering the aorta at the PDA. Not so for the lower extremities whose arteries branch after the PDA and so receive low oxygen blood. Hence in Eisenmenger syndrome patients, only the feet are cyanosed.",True,Patent Ductus Arteriosus,,,,
338d8730-fb8e-4828-8430-57f99e232ab8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,Atrioventricular Canal,False,Atrioventricular Canal,,,,
abd722ce-85e6-4fc7-bbc3-e5289b86f49f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
abd722ce-85e6-4fc7-bbc3-e5289b86f49f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
abd722ce-85e6-4fc7-bbc3-e5289b86f49f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
abd722ce-85e6-4fc7-bbc3-e5289b86f49f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
abd722ce-85e6-4fc7-bbc3-e5289b86f49f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
abd722ce-85e6-4fc7-bbc3-e5289b86f49f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
abd722ce-85e6-4fc7-bbc3-e5289b86f49f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
abd722ce-85e6-4fc7-bbc3-e5289b86f49f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
abd722ce-85e6-4fc7-bbc3-e5289b86f49f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
fc4359a7-39b7-4361-a225-543f60a1b26b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The malformed valves allow regurgitation, and the unrestricted interventricular communication allow a profound left–right shunt. This leads to volume overload in the pulmonary circulation, and heart failure will be produced if there is no correction. Pulmonary artery hypertension (PAH) and premature development of pulmonary vascular obstructive disease are other common outcomes.",True,Atrioventricular Canal,,,,
8201ef08-2465-4de2-b5d7-452781efe825,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,Truncus Arteriosus,False,Truncus Arteriosus,,,,
ff8b1790-6041-40e0-8779-17d5fe2b1d95,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
ff8b1790-6041-40e0-8779-17d5fe2b1d95,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
ff8b1790-6041-40e0-8779-17d5fe2b1d95,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
ff8b1790-6041-40e0-8779-17d5fe2b1d95,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
ff8b1790-6041-40e0-8779-17d5fe2b1d95,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
ff8b1790-6041-40e0-8779-17d5fe2b1d95,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
ff8b1790-6041-40e0-8779-17d5fe2b1d95,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
ff8b1790-6041-40e0-8779-17d5fe2b1d95,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
ff8b1790-6041-40e0-8779-17d5fe2b1d95,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
f9ef1c41-bfd6-4190-8676-5e44f7f2cff4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"The underlying issues with TA are 1) mixing of blood from the left (saturated) and right heart (unsaturated), and 2) the common valve can allow regurgitation. In utero the high pulmonary vascular resistance means most blood exiting the heart goes through the aorta and cardiac output is rarely affected. At birth mild cyanosis can be produced by the mixing of blood from the left and right heart, but as pulmonary vascular resistance remains high in the first few days of life, cardiac output my be maintained. As pulmonary vascular resistance continues to fall in the first few weeks of life, a significant left–right shunt can become established as more left ventricular blood finds it “easier” to ascend up the pulmonary artery. Similar to a VSD, this leads to volume overload in the pulmonary circulation and eventually heart failure. The heart failure has a more rapid onset in TA than VSD if the common valve allows regurgitation. The regurgitation lowers end-diastolic ventricular volumes, so cardiac work to maintain cardiac output increases and promotes myocardial ischemia. Add to this the left–right shunt (as seen in VSD) and heart failure is more likely.",True,Truncus Arteriosus,,,,
dc352984-2192-4d18-98f0-fd6c1bcdbc0a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,Text,False,Text,,,,
97f3e456-e5a3-4cd5-a878-bfaac6ed7664,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Bhansali, Suneet, and Colin Phoon. Truncus Arteriosis. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK534774/, CC BY 4.0.",True,Text,,,,
c8520c1b-2e56-42f0-8fac-fb7efbd47c52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Cunningham, Jonathan W., and David W. Brown. “Congenital Heart Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, edited by Leonard S. Lilly, Chapter 16. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2012.",True,Text,,,,
634b1c4d-dd46-44e2-a590-b78ae40cf349,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Dakkak, Wael, and Tony I. Oliver. Ventricular Septal Defect. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK470330/, CC BY 4.0.",True,Text,,,,
00a8aac4-b753-4cbb-93db-b8e271d94a43,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Diaz-Frias, Josua, and Melissa Guillaume. Tetralogy of Fallot. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK513288/, CC BY 4.0.",True,Text,,,,
6ba3e9ff-84ae-41e0-abee-8b874d7162e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Gillam-Krakauer, Maria, and Kunal Mahajan. Patent Ductus Ateriosus. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430758/, CC BY 4.0.",True,Text,,,,
db5fe35e-f936-40f0-aee5-47093936b38a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Law, Mark A., and Vijai  S. Tivakaran. Coarctation of the Aorta. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430913/, CC BY 4.0.",True,Text,,,,
75457089-945f-42b8-9a2c-c5ee15595367,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Menillo, Alexandra M., Lawrence S. Lee, and Anthony L. Pearson-Shaver. Atrial Septal Defect. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK535440/, CC BY 4.0.",True,Text,,,,
97575db7-20c6-4705-82db-04a1550dbc77,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Szymanski, Michael W., Sheila M. Moore, Stacy M. Kritzmire, and Amandeep Goyal. Transposition of the Great Arteries. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430758/, CC BY 4.0.",True,Text,,,,
a044b84c-2cbf-475f-b5a6-71cd207a7f38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-4,"Umapathi, Krishna Kishore, and Pradyumna Agasthi. Atrioventricular Canal Defects. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK557511/, CC BY 4.0.",True,Text,,,,
a9db01ff-8dcb-4cb4-9e87-d70c897f6838,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,Embryology,False,Embryology,,,,
da660423-899e-4c2a-ad85-044fd4053370,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,The most common atrial septal defects arise from:,False,The most common atrial septal defects arise from:,,,,
cc347ab8-4f90-4e3b-887d-d0afd9629e88,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"A patent foramen ovale (20 percent of the population) is not a true ASD as no tissue is missing and the remaining tissue acts as a one-way valve, so a PFO does not have the same pathophysiology as a true ASD. ASDs are common in infants with Down syndrome, as are VSDs.",True,The most common atrial septal defects arise from:,,,,
67041c3d-a20d-4271-b29a-460d680d7422,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,Pathophysiology,False,Pathophysiology,,,,
b830c72c-3945-4e0b-8aef-d0291bad9e9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
b830c72c-3945-4e0b-8aef-d0291bad9e9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
b830c72c-3945-4e0b-8aef-d0291bad9e9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
b830c72c-3945-4e0b-8aef-d0291bad9e9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
b830c72c-3945-4e0b-8aef-d0291bad9e9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
b830c72c-3945-4e0b-8aef-d0291bad9e9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
b830c72c-3945-4e0b-8aef-d0291bad9e9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
b830c72c-3945-4e0b-8aef-d0291bad9e9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
b830c72c-3945-4e0b-8aef-d0291bad9e9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
8f6d2595-294f-4f76-94a7-e2ec26d11002,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,Ventricular Septal Defect (VSD),False,Ventricular Septal Defect (VSD),,,,
dc501d35-7806-4248-b11b-e793ccd075b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Most ventricular septal defects arise from membraneous portion of the septum (70 percent), while others form in the muscular portion (20 percent); less frequently they occur near the aortic or AV valves.",True,Ventricular Septal Defect (VSD),,,,
219e88c9-5145-4167-8213-632b98b75ee1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
219e88c9-5145-4167-8213-632b98b75ee1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
219e88c9-5145-4167-8213-632b98b75ee1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
219e88c9-5145-4167-8213-632b98b75ee1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
219e88c9-5145-4167-8213-632b98b75ee1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
219e88c9-5145-4167-8213-632b98b75ee1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
219e88c9-5145-4167-8213-632b98b75ee1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
219e88c9-5145-4167-8213-632b98b75ee1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
219e88c9-5145-4167-8213-632b98b75ee1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
df1f3c46-4e38-4b72-bd7c-8fbd5861ac68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
df1f3c46-4e38-4b72-bd7c-8fbd5861ac68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
df1f3c46-4e38-4b72-bd7c-8fbd5861ac68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
df1f3c46-4e38-4b72-bd7c-8fbd5861ac68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
df1f3c46-4e38-4b72-bd7c-8fbd5861ac68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
df1f3c46-4e38-4b72-bd7c-8fbd5861ac68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
df1f3c46-4e38-4b72-bd7c-8fbd5861ac68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
df1f3c46-4e38-4b72-bd7c-8fbd5861ac68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
df1f3c46-4e38-4b72-bd7c-8fbd5861ac68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
ea88e4a1-a0dd-450d-85e5-5ea0b0410969,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,Coarctation of the Aorta,False,Coarctation of the Aorta,,,,
4ab37554-f774-4e26-b705-4a4af80a32e3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
4ab37554-f774-4e26-b705-4a4af80a32e3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
4ab37554-f774-4e26-b705-4a4af80a32e3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
4ab37554-f774-4e26-b705-4a4af80a32e3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
4ab37554-f774-4e26-b705-4a4af80a32e3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
4ab37554-f774-4e26-b705-4a4af80a32e3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
4ab37554-f774-4e26-b705-4a4af80a32e3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
4ab37554-f774-4e26-b705-4a4af80a32e3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
4ab37554-f774-4e26-b705-4a4af80a32e3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
3119fa78-8b70-4b7b-bdb8-379666f803f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The diminished lumen causes increased afterload on the left ventricle. Vessels branching off the aorta before the coarctation can receive normal blood flow, so the head (carotid) and upper extremities (subclavian) are usually properly perfused whereas branching arteries after the coarctation may be underperfused. Consequently, differential cyanosis is a possible manifestation.",True,Coarctation of the Aorta,,,,
a095ea21-0d39-4c0c-b1d9-082449115856,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,Tetralogy of Fallot (ToF),False,Tetralogy of Fallot (ToF),,,,
85c969cc-7b16-46a1-8f89-88aa124f0bdb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,In Tetralogy of Fallot (ToF) the outflow tract (infundibular) portion of the interventricular septum is displaced. This single defect leads to four defects:,True,Tetralogy of Fallot (ToF),,,,
9a809cc9-4dbe-406f-ac7a-751abf5e4631,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Other defects can be associated with ToF, but the defects listed above lead this to be the most common form of cyanotic congenital heart disease.",True,Tetralogy of Fallot (ToF),,,,
a012c0af-3dc0-4f69-a8ae-1deba259e186,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
a012c0af-3dc0-4f69-a8ae-1deba259e186,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
a012c0af-3dc0-4f69-a8ae-1deba259e186,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
a012c0af-3dc0-4f69-a8ae-1deba259e186,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
a012c0af-3dc0-4f69-a8ae-1deba259e186,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
a012c0af-3dc0-4f69-a8ae-1deba259e186,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
a012c0af-3dc0-4f69-a8ae-1deba259e186,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
a012c0af-3dc0-4f69-a8ae-1deba259e186,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
a012c0af-3dc0-4f69-a8ae-1deba259e186,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
48b4ebbd-b107-4ad4-9230-16c01dc9f402,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,Transposition of the Great Arteries,False,Transposition of the Great Arteries,,,,
19fe0eb8-c6fc-4d33-b30e-8c422b8c374b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Although not completely understood, it is thought that failure of the aortic-pulmonary septum to spiral during development results in the great vessels coming off the wrong ventricles—the aorta exits the right, and the pulmonary artery exits the left. Other theories exist.",True,Transposition of the Great Arteries,,,,
7c02a6b6-e6cb-480c-bd04-4036b23733a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
7c02a6b6-e6cb-480c-bd04-4036b23733a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
7c02a6b6-e6cb-480c-bd04-4036b23733a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
7c02a6b6-e6cb-480c-bd04-4036b23733a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
7c02a6b6-e6cb-480c-bd04-4036b23733a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
7c02a6b6-e6cb-480c-bd04-4036b23733a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
7c02a6b6-e6cb-480c-bd04-4036b23733a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
7c02a6b6-e6cb-480c-bd04-4036b23733a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
7c02a6b6-e6cb-480c-bd04-4036b23733a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
dcba12a7-2aa7-4503-a6af-a0970bc4ac8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,Patent Ductus Arteriosus,False,Patent Ductus Arteriosus,,,,
f42801fc-e87d-4182-a572-9de529c0e830,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The ductus arteriosus is part of the fetal circulation allowing blood in the pulmonary artery to bypass the nonfunctional, high resistance lungs and instead traverse into the aorta and systemic circulation. The ductus should close at birth, and failure to do so leaves a patent ductus arteriosus (PDA).",True,Patent Ductus Arteriosus,,,,
c30523ae-ded2-4463-bb58-47f9430ce2a3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
c30523ae-ded2-4463-bb58-47f9430ce2a3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
c30523ae-ded2-4463-bb58-47f9430ce2a3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
c30523ae-ded2-4463-bb58-47f9430ce2a3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
c30523ae-ded2-4463-bb58-47f9430ce2a3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
c30523ae-ded2-4463-bb58-47f9430ce2a3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
c30523ae-ded2-4463-bb58-47f9430ce2a3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
c30523ae-ded2-4463-bb58-47f9430ce2a3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
c30523ae-ded2-4463-bb58-47f9430ce2a3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
c06ab66d-65e7-44a4-8516-733fcff96b03,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The consequences of this are that a greater volume of blood reenters the pulmonary circulation, the left atria, and the left ventricle. Consequently the compartments of the left heart can eventually fail through volume overload. When the left heart fails, the shunt through the PDA can be reversed, and desaturated blood destined for the pulmonary circulation can end up passing through the PDA to the aorta instead—this reversal later in life is called Eisenmenger syndrome. In Eisenmenger’s the upper extremities receive uncontaminated, saturated blood, as their branching arteries are upstream of the desaturated blood entering the aorta at the PDA. Not so for the lower extremities whose arteries branch after the PDA and so receive low oxygen blood. Hence in Eisenmenger syndrome patients, only the feet are cyanosed.",True,Patent Ductus Arteriosus,,,,
3de30f42-ea35-41d8-a579-8d1a8116f7cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,Atrioventricular Canal,False,Atrioventricular Canal,,,,
e66e95a8-8e12-45f9-9c4d-e6e435ef4d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
e66e95a8-8e12-45f9-9c4d-e6e435ef4d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
e66e95a8-8e12-45f9-9c4d-e6e435ef4d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
e66e95a8-8e12-45f9-9c4d-e6e435ef4d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
e66e95a8-8e12-45f9-9c4d-e6e435ef4d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
e66e95a8-8e12-45f9-9c4d-e6e435ef4d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
e66e95a8-8e12-45f9-9c4d-e6e435ef4d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
e66e95a8-8e12-45f9-9c4d-e6e435ef4d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
e66e95a8-8e12-45f9-9c4d-e6e435ef4d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
04c12275-d499-44e5-abed-bcaf60a4a848,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The malformed valves allow regurgitation, and the unrestricted interventricular communication allow a profound left–right shunt. This leads to volume overload in the pulmonary circulation, and heart failure will be produced if there is no correction. Pulmonary artery hypertension (PAH) and premature development of pulmonary vascular obstructive disease are other common outcomes.",True,Atrioventricular Canal,,,,
c1a6cb02-62c8-4c87-9cc6-56a3ba64a7f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,Truncus Arteriosus,False,Truncus Arteriosus,,,,
31224045-25e6-4e71-a870-21746bebf8e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
31224045-25e6-4e71-a870-21746bebf8e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
31224045-25e6-4e71-a870-21746bebf8e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
31224045-25e6-4e71-a870-21746bebf8e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
31224045-25e6-4e71-a870-21746bebf8e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
31224045-25e6-4e71-a870-21746bebf8e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
31224045-25e6-4e71-a870-21746bebf8e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
31224045-25e6-4e71-a870-21746bebf8e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
31224045-25e6-4e71-a870-21746bebf8e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
8f052ee3-a30e-4546-ad1b-03e2e4ee3155,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"The underlying issues with TA are 1) mixing of blood from the left (saturated) and right heart (unsaturated), and 2) the common valve can allow regurgitation. In utero the high pulmonary vascular resistance means most blood exiting the heart goes through the aorta and cardiac output is rarely affected. At birth mild cyanosis can be produced by the mixing of blood from the left and right heart, but as pulmonary vascular resistance remains high in the first few days of life, cardiac output my be maintained. As pulmonary vascular resistance continues to fall in the first few weeks of life, a significant left–right shunt can become established as more left ventricular blood finds it “easier” to ascend up the pulmonary artery. Similar to a VSD, this leads to volume overload in the pulmonary circulation and eventually heart failure. The heart failure has a more rapid onset in TA than VSD if the common valve allows regurgitation. The regurgitation lowers end-diastolic ventricular volumes, so cardiac work to maintain cardiac output increases and promotes myocardial ischemia. Add to this the left–right shunt (as seen in VSD) and heart failure is more likely.",True,Truncus Arteriosus,,,,
d4747340-89c7-425a-824f-f5497745b935,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,Text,False,Text,,,,
b63c97f2-0b97-4204-88de-fbda99347846,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Bhansali, Suneet, and Colin Phoon. Truncus Arteriosis. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK534774/, CC BY 4.0.",True,Text,,,,
8873c474-b253-4d09-91ce-9a50ce00558d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Cunningham, Jonathan W., and David W. Brown. “Congenital Heart Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, edited by Leonard S. Lilly, Chapter 16. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2012.",True,Text,,,,
67ce4357-5520-4ae3-8f6c-175632276b87,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Dakkak, Wael, and Tony I. Oliver. Ventricular Septal Defect. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK470330/, CC BY 4.0.",True,Text,,,,
53669914-d1cf-4165-b76e-fd340b489e57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Diaz-Frias, Josua, and Melissa Guillaume. Tetralogy of Fallot. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK513288/, CC BY 4.0.",True,Text,,,,
6bc7e2b5-6638-4b29-950f-0ce02dcd5a76,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Gillam-Krakauer, Maria, and Kunal Mahajan. Patent Ductus Ateriosus. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430758/, CC BY 4.0.",True,Text,,,,
69586906-e5b4-461a-9d9f-b750a96c911e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Law, Mark A., and Vijai  S. Tivakaran. Coarctation of the Aorta. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430913/, CC BY 4.0.",True,Text,,,,
a02c79e2-e945-4100-8825-cb5b17f401fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Menillo, Alexandra M., Lawrence S. Lee, and Anthony L. Pearson-Shaver. Atrial Septal Defect. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK535440/, CC BY 4.0.",True,Text,,,,
60041bd5-8616-49d3-93bd-1a67001736e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Szymanski, Michael W., Sheila M. Moore, Stacy M. Kritzmire, and Amandeep Goyal. Transposition of the Great Arteries. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430758/, CC BY 4.0.",True,Text,,,,
72d59a59-b5c5-45a1-970f-e4587b720de3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-3,"Umapathi, Krishna Kishore, and Pradyumna Agasthi. Atrioventricular Canal Defects. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK557511/, CC BY 4.0.",True,Text,,,,
9a5375fa-7d82-4110-8d36-2c20ace78277,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,Embryology,False,Embryology,,,,
91523108-1510-4fa3-82d1-4a17861fdabb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,The most common atrial septal defects arise from:,False,The most common atrial septal defects arise from:,,,,
467735c6-a600-4df4-92cb-35c39e164483,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"A patent foramen ovale (20 percent of the population) is not a true ASD as no tissue is missing and the remaining tissue acts as a one-way valve, so a PFO does not have the same pathophysiology as a true ASD. ASDs are common in infants with Down syndrome, as are VSDs.",True,The most common atrial septal defects arise from:,,,,
ea539cd9-bccf-4ce3-acfd-0b14be58897a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,Pathophysiology,False,Pathophysiology,,,,
c6e1de51-ad98-4b6b-b781-51d7984b9684,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
c6e1de51-ad98-4b6b-b781-51d7984b9684,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
c6e1de51-ad98-4b6b-b781-51d7984b9684,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
c6e1de51-ad98-4b6b-b781-51d7984b9684,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
c6e1de51-ad98-4b6b-b781-51d7984b9684,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
c6e1de51-ad98-4b6b-b781-51d7984b9684,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
c6e1de51-ad98-4b6b-b781-51d7984b9684,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
c6e1de51-ad98-4b6b-b781-51d7984b9684,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
c6e1de51-ad98-4b6b-b781-51d7984b9684,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
e289bdb4-ce10-41ee-b13f-3a18be2a7d5b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,Ventricular Septal Defect (VSD),False,Ventricular Septal Defect (VSD),,,,
1f59880c-cf84-40c7-84cd-b915f403f704,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Most ventricular septal defects arise from membraneous portion of the septum (70 percent), while others form in the muscular portion (20 percent); less frequently they occur near the aortic or AV valves.",True,Ventricular Septal Defect (VSD),,,,
0013cf30-21b0-4b78-8625-65a7dd94214a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
0013cf30-21b0-4b78-8625-65a7dd94214a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
0013cf30-21b0-4b78-8625-65a7dd94214a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
0013cf30-21b0-4b78-8625-65a7dd94214a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
0013cf30-21b0-4b78-8625-65a7dd94214a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
0013cf30-21b0-4b78-8625-65a7dd94214a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
0013cf30-21b0-4b78-8625-65a7dd94214a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
0013cf30-21b0-4b78-8625-65a7dd94214a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
0013cf30-21b0-4b78-8625-65a7dd94214a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
9ea29e10-9172-4d95-9552-53b568952558,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
9ea29e10-9172-4d95-9552-53b568952558,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
9ea29e10-9172-4d95-9552-53b568952558,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
9ea29e10-9172-4d95-9552-53b568952558,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
9ea29e10-9172-4d95-9552-53b568952558,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
9ea29e10-9172-4d95-9552-53b568952558,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
9ea29e10-9172-4d95-9552-53b568952558,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
9ea29e10-9172-4d95-9552-53b568952558,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
9ea29e10-9172-4d95-9552-53b568952558,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
8a9652bd-b3e6-4d72-af09-9cf3f9e6cb3e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,Coarctation of the Aorta,False,Coarctation of the Aorta,,,,
b46de6b6-62f6-443e-bb0f-5cb6e0efd7d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
b46de6b6-62f6-443e-bb0f-5cb6e0efd7d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
b46de6b6-62f6-443e-bb0f-5cb6e0efd7d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
b46de6b6-62f6-443e-bb0f-5cb6e0efd7d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
b46de6b6-62f6-443e-bb0f-5cb6e0efd7d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
b46de6b6-62f6-443e-bb0f-5cb6e0efd7d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
b46de6b6-62f6-443e-bb0f-5cb6e0efd7d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
b46de6b6-62f6-443e-bb0f-5cb6e0efd7d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
b46de6b6-62f6-443e-bb0f-5cb6e0efd7d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
5b6ed972-490e-426e-925f-010d092923df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The diminished lumen causes increased afterload on the left ventricle. Vessels branching off the aorta before the coarctation can receive normal blood flow, so the head (carotid) and upper extremities (subclavian) are usually properly perfused whereas branching arteries after the coarctation may be underperfused. Consequently, differential cyanosis is a possible manifestation.",True,Coarctation of the Aorta,,,,
eb8610b4-374f-41c7-88f2-45189734a9c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,Tetralogy of Fallot (ToF),False,Tetralogy of Fallot (ToF),,,,
247e3bc1-03bf-4054-bb2c-09d19b8b80f9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,In Tetralogy of Fallot (ToF) the outflow tract (infundibular) portion of the interventricular septum is displaced. This single defect leads to four defects:,True,Tetralogy of Fallot (ToF),,,,
db541a30-3ff4-4dc5-b9b6-e0e6de3ee010,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Other defects can be associated with ToF, but the defects listed above lead this to be the most common form of cyanotic congenital heart disease.",True,Tetralogy of Fallot (ToF),,,,
7c8f0a98-94bd-469c-a6dd-0ac311da79c1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
7c8f0a98-94bd-469c-a6dd-0ac311da79c1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
7c8f0a98-94bd-469c-a6dd-0ac311da79c1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
7c8f0a98-94bd-469c-a6dd-0ac311da79c1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
7c8f0a98-94bd-469c-a6dd-0ac311da79c1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
7c8f0a98-94bd-469c-a6dd-0ac311da79c1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
7c8f0a98-94bd-469c-a6dd-0ac311da79c1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
7c8f0a98-94bd-469c-a6dd-0ac311da79c1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
7c8f0a98-94bd-469c-a6dd-0ac311da79c1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
919c9e23-b274-4289-9f6c-045c29a903b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,Transposition of the Great Arteries,False,Transposition of the Great Arteries,,,,
a464dd5c-f4c6-4815-a998-c93fcc17906b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Although not completely understood, it is thought that failure of the aortic-pulmonary septum to spiral during development results in the great vessels coming off the wrong ventricles—the aorta exits the right, and the pulmonary artery exits the left. Other theories exist.",True,Transposition of the Great Arteries,,,,
f074aab5-9a5b-4859-87aa-6c38f3a366ea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
f074aab5-9a5b-4859-87aa-6c38f3a366ea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
f074aab5-9a5b-4859-87aa-6c38f3a366ea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
f074aab5-9a5b-4859-87aa-6c38f3a366ea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
f074aab5-9a5b-4859-87aa-6c38f3a366ea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
f074aab5-9a5b-4859-87aa-6c38f3a366ea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
f074aab5-9a5b-4859-87aa-6c38f3a366ea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
f074aab5-9a5b-4859-87aa-6c38f3a366ea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
f074aab5-9a5b-4859-87aa-6c38f3a366ea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
643fe4d0-4fd3-4def-95a7-a38f6d25ecfe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,Patent Ductus Arteriosus,False,Patent Ductus Arteriosus,,,,
ea60865e-86d6-41b4-a1b6-e5bc80196384,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The ductus arteriosus is part of the fetal circulation allowing blood in the pulmonary artery to bypass the nonfunctional, high resistance lungs and instead traverse into the aorta and systemic circulation. The ductus should close at birth, and failure to do so leaves a patent ductus arteriosus (PDA).",True,Patent Ductus Arteriosus,,,,
7aaecfbd-81c8-4c7e-8e7a-5310b07acc77,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
7aaecfbd-81c8-4c7e-8e7a-5310b07acc77,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
7aaecfbd-81c8-4c7e-8e7a-5310b07acc77,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
7aaecfbd-81c8-4c7e-8e7a-5310b07acc77,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
7aaecfbd-81c8-4c7e-8e7a-5310b07acc77,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
7aaecfbd-81c8-4c7e-8e7a-5310b07acc77,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
7aaecfbd-81c8-4c7e-8e7a-5310b07acc77,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
7aaecfbd-81c8-4c7e-8e7a-5310b07acc77,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
7aaecfbd-81c8-4c7e-8e7a-5310b07acc77,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
bd6a9be0-ade9-4b28-81b7-26dea8c8e202,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The consequences of this are that a greater volume of blood reenters the pulmonary circulation, the left atria, and the left ventricle. Consequently the compartments of the left heart can eventually fail through volume overload. When the left heart fails, the shunt through the PDA can be reversed, and desaturated blood destined for the pulmonary circulation can end up passing through the PDA to the aorta instead—this reversal later in life is called Eisenmenger syndrome. In Eisenmenger’s the upper extremities receive uncontaminated, saturated blood, as their branching arteries are upstream of the desaturated blood entering the aorta at the PDA. Not so for the lower extremities whose arteries branch after the PDA and so receive low oxygen blood. Hence in Eisenmenger syndrome patients, only the feet are cyanosed.",True,Patent Ductus Arteriosus,,,,
5b0f0622-bdee-424c-9daa-f6c9361a066f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,Atrioventricular Canal,False,Atrioventricular Canal,,,,
6e8d0f13-eec3-4a89-86ef-8d3e42e61ad7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
6e8d0f13-eec3-4a89-86ef-8d3e42e61ad7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
6e8d0f13-eec3-4a89-86ef-8d3e42e61ad7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
6e8d0f13-eec3-4a89-86ef-8d3e42e61ad7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
6e8d0f13-eec3-4a89-86ef-8d3e42e61ad7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
6e8d0f13-eec3-4a89-86ef-8d3e42e61ad7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
6e8d0f13-eec3-4a89-86ef-8d3e42e61ad7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
6e8d0f13-eec3-4a89-86ef-8d3e42e61ad7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
6e8d0f13-eec3-4a89-86ef-8d3e42e61ad7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
79892172-1cfb-401d-9176-668f1ed34530,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The malformed valves allow regurgitation, and the unrestricted interventricular communication allow a profound left–right shunt. This leads to volume overload in the pulmonary circulation, and heart failure will be produced if there is no correction. Pulmonary artery hypertension (PAH) and premature development of pulmonary vascular obstructive disease are other common outcomes.",True,Atrioventricular Canal,,,,
56694301-63e9-4558-9acb-3938acc68107,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,Truncus Arteriosus,False,Truncus Arteriosus,,,,
45e92ae7-4102-4ee3-9886-14c471f36069,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
45e92ae7-4102-4ee3-9886-14c471f36069,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
45e92ae7-4102-4ee3-9886-14c471f36069,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
45e92ae7-4102-4ee3-9886-14c471f36069,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
45e92ae7-4102-4ee3-9886-14c471f36069,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
45e92ae7-4102-4ee3-9886-14c471f36069,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
45e92ae7-4102-4ee3-9886-14c471f36069,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
45e92ae7-4102-4ee3-9886-14c471f36069,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
45e92ae7-4102-4ee3-9886-14c471f36069,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
a1b58b62-9b2f-4032-8f12-ba50b76e85e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"The underlying issues with TA are 1) mixing of blood from the left (saturated) and right heart (unsaturated), and 2) the common valve can allow regurgitation. In utero the high pulmonary vascular resistance means most blood exiting the heart goes through the aorta and cardiac output is rarely affected. At birth mild cyanosis can be produced by the mixing of blood from the left and right heart, but as pulmonary vascular resistance remains high in the first few days of life, cardiac output my be maintained. As pulmonary vascular resistance continues to fall in the first few weeks of life, a significant left–right shunt can become established as more left ventricular blood finds it “easier” to ascend up the pulmonary artery. Similar to a VSD, this leads to volume overload in the pulmonary circulation and eventually heart failure. The heart failure has a more rapid onset in TA than VSD if the common valve allows regurgitation. The regurgitation lowers end-diastolic ventricular volumes, so cardiac work to maintain cardiac output increases and promotes myocardial ischemia. Add to this the left–right shunt (as seen in VSD) and heart failure is more likely.",True,Truncus Arteriosus,,,,
fea28578-1640-4c9f-9edb-dd25cb642a58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,Text,False,Text,,,,
f14cc461-641f-4585-950f-cf1086619498,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Bhansali, Suneet, and Colin Phoon. Truncus Arteriosis. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK534774/, CC BY 4.0.",True,Text,,,,
1b49884e-9ada-4807-bd52-18446b193d1c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Cunningham, Jonathan W., and David W. Brown. “Congenital Heart Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, edited by Leonard S. Lilly, Chapter 16. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2012.",True,Text,,,,
25cc8df0-d831-43fa-b25b-d9e95ba740ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Dakkak, Wael, and Tony I. Oliver. Ventricular Septal Defect. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK470330/, CC BY 4.0.",True,Text,,,,
90bbdd41-5335-421f-a2c6-17d0cf9f3abe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Diaz-Frias, Josua, and Melissa Guillaume. Tetralogy of Fallot. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK513288/, CC BY 4.0.",True,Text,,,,
1ee521a9-5fbc-4d6a-8f06-d5a9c7dce31c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Gillam-Krakauer, Maria, and Kunal Mahajan. Patent Ductus Ateriosus. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430758/, CC BY 4.0.",True,Text,,,,
5d96b578-4420-4933-874a-8289080c86ba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Law, Mark A., and Vijai  S. Tivakaran. Coarctation of the Aorta. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430913/, CC BY 4.0.",True,Text,,,,
0a9d55cb-dce0-4148-8608-26ae4e6b2442,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Menillo, Alexandra M., Lawrence S. Lee, and Anthony L. Pearson-Shaver. Atrial Septal Defect. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK535440/, CC BY 4.0.",True,Text,,,,
e4e5aed6-8fa8-497e-88e1-357505c6d062,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Szymanski, Michael W., Sheila M. Moore, Stacy M. Kritzmire, and Amandeep Goyal. Transposition of the Great Arteries. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430758/, CC BY 4.0.",True,Text,,,,
d5f4e177-b67c-434e-ba0b-75dc35fe7a14,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-2,"Umapathi, Krishna Kishore, and Pradyumna Agasthi. Atrioventricular Canal Defects. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK557511/, CC BY 4.0.",True,Text,,,,
c8d068cb-bce9-4889-88cb-352b13e2b5c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,Embryology,False,Embryology,,,,
1781a248-b320-4bd8-ac66-18fd6951dc97,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,The most common atrial septal defects arise from:,False,The most common atrial septal defects arise from:,,,,
8ede4b31-06c8-4e29-b9f5-a9ed6d21b9a2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"A patent foramen ovale (20 percent of the population) is not a true ASD as no tissue is missing and the remaining tissue acts as a one-way valve, so a PFO does not have the same pathophysiology as a true ASD. ASDs are common in infants with Down syndrome, as are VSDs.",True,The most common atrial septal defects arise from:,,,,
224b90f1-8198-44ab-a038-65bf9aa0adf2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,Pathophysiology,False,Pathophysiology,,,,
a0db7ed2-74f4-47f2-bc2f-9eafdb0592e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
a0db7ed2-74f4-47f2-bc2f-9eafdb0592e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
a0db7ed2-74f4-47f2-bc2f-9eafdb0592e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
a0db7ed2-74f4-47f2-bc2f-9eafdb0592e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
a0db7ed2-74f4-47f2-bc2f-9eafdb0592e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
a0db7ed2-74f4-47f2-bc2f-9eafdb0592e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
a0db7ed2-74f4-47f2-bc2f-9eafdb0592e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
a0db7ed2-74f4-47f2-bc2f-9eafdb0592e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
a0db7ed2-74f4-47f2-bc2f-9eafdb0592e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
94dbe99f-ac23-4a38-8b78-d027a9085e44,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,Ventricular Septal Defect (VSD),False,Ventricular Septal Defect (VSD),,,,
15f487e9-7b34-4fd4-a5c3-afdfcacd35f9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Most ventricular septal defects arise from membraneous portion of the septum (70 percent), while others form in the muscular portion (20 percent); less frequently they occur near the aortic or AV valves.",True,Ventricular Septal Defect (VSD),,,,
c30b6766-6bfa-46e5-920a-426e22c0a260,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
c30b6766-6bfa-46e5-920a-426e22c0a260,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
c30b6766-6bfa-46e5-920a-426e22c0a260,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
c30b6766-6bfa-46e5-920a-426e22c0a260,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
c30b6766-6bfa-46e5-920a-426e22c0a260,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
c30b6766-6bfa-46e5-920a-426e22c0a260,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
c30b6766-6bfa-46e5-920a-426e22c0a260,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
c30b6766-6bfa-46e5-920a-426e22c0a260,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
c30b6766-6bfa-46e5-920a-426e22c0a260,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
553c787e-92da-421a-bb93-6b210c78fc36,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
553c787e-92da-421a-bb93-6b210c78fc36,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
553c787e-92da-421a-bb93-6b210c78fc36,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
553c787e-92da-421a-bb93-6b210c78fc36,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
553c787e-92da-421a-bb93-6b210c78fc36,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
553c787e-92da-421a-bb93-6b210c78fc36,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
553c787e-92da-421a-bb93-6b210c78fc36,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
553c787e-92da-421a-bb93-6b210c78fc36,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
553c787e-92da-421a-bb93-6b210c78fc36,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
3ec064d6-7537-4512-9625-4674135fa48a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,Coarctation of the Aorta,False,Coarctation of the Aorta,,,,
54a824c9-134d-4d5d-8794-8e9be616a2f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
54a824c9-134d-4d5d-8794-8e9be616a2f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
54a824c9-134d-4d5d-8794-8e9be616a2f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
54a824c9-134d-4d5d-8794-8e9be616a2f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
54a824c9-134d-4d5d-8794-8e9be616a2f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
54a824c9-134d-4d5d-8794-8e9be616a2f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
54a824c9-134d-4d5d-8794-8e9be616a2f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
54a824c9-134d-4d5d-8794-8e9be616a2f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
54a824c9-134d-4d5d-8794-8e9be616a2f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
a95ea82f-c161-4432-91b8-01407021274a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The diminished lumen causes increased afterload on the left ventricle. Vessels branching off the aorta before the coarctation can receive normal blood flow, so the head (carotid) and upper extremities (subclavian) are usually properly perfused whereas branching arteries after the coarctation may be underperfused. Consequently, differential cyanosis is a possible manifestation.",True,Coarctation of the Aorta,,,,
a1eb6ef6-98e6-4258-a181-eada756c8202,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,Tetralogy of Fallot (ToF),False,Tetralogy of Fallot (ToF),,,,
d9121f2a-6fd7-4042-aac2-c8776c523421,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,In Tetralogy of Fallot (ToF) the outflow tract (infundibular) portion of the interventricular septum is displaced. This single defect leads to four defects:,True,Tetralogy of Fallot (ToF),,,,
ceca9d6a-2bb8-4778-87ee-aac1dd927b44,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Other defects can be associated with ToF, but the defects listed above lead this to be the most common form of cyanotic congenital heart disease.",True,Tetralogy of Fallot (ToF),,,,
4e0478cb-bb0a-467a-86a6-0410e4f4265c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
4e0478cb-bb0a-467a-86a6-0410e4f4265c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
4e0478cb-bb0a-467a-86a6-0410e4f4265c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
4e0478cb-bb0a-467a-86a6-0410e4f4265c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
4e0478cb-bb0a-467a-86a6-0410e4f4265c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
4e0478cb-bb0a-467a-86a6-0410e4f4265c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
4e0478cb-bb0a-467a-86a6-0410e4f4265c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
4e0478cb-bb0a-467a-86a6-0410e4f4265c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
4e0478cb-bb0a-467a-86a6-0410e4f4265c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
ef62c99f-a4b0-4b88-a8ae-c17f3e722081,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,Transposition of the Great Arteries,False,Transposition of the Great Arteries,,,,
c9087e28-7803-4382-b11e-328b65bfc235,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Although not completely understood, it is thought that failure of the aortic-pulmonary septum to spiral during development results in the great vessels coming off the wrong ventricles—the aorta exits the right, and the pulmonary artery exits the left. Other theories exist.",True,Transposition of the Great Arteries,,,,
fa3d7e87-53ef-4b41-8a0e-eda6c9a097d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
fa3d7e87-53ef-4b41-8a0e-eda6c9a097d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
fa3d7e87-53ef-4b41-8a0e-eda6c9a097d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
fa3d7e87-53ef-4b41-8a0e-eda6c9a097d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
fa3d7e87-53ef-4b41-8a0e-eda6c9a097d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
fa3d7e87-53ef-4b41-8a0e-eda6c9a097d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
fa3d7e87-53ef-4b41-8a0e-eda6c9a097d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
fa3d7e87-53ef-4b41-8a0e-eda6c9a097d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
fa3d7e87-53ef-4b41-8a0e-eda6c9a097d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
e8ee0487-37bd-49b1-881e-215ae88edd0f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,Patent Ductus Arteriosus,False,Patent Ductus Arteriosus,,,,
797dd71f-d6a9-443c-a40f-2ca8aac9a2b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The ductus arteriosus is part of the fetal circulation allowing blood in the pulmonary artery to bypass the nonfunctional, high resistance lungs and instead traverse into the aorta and systemic circulation. The ductus should close at birth, and failure to do so leaves a patent ductus arteriosus (PDA).",True,Patent Ductus Arteriosus,,,,
c1019c65-de87-42fb-ad73-fde654010375,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
c1019c65-de87-42fb-ad73-fde654010375,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
c1019c65-de87-42fb-ad73-fde654010375,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
c1019c65-de87-42fb-ad73-fde654010375,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
c1019c65-de87-42fb-ad73-fde654010375,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
c1019c65-de87-42fb-ad73-fde654010375,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
c1019c65-de87-42fb-ad73-fde654010375,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
c1019c65-de87-42fb-ad73-fde654010375,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
c1019c65-de87-42fb-ad73-fde654010375,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
7300d1ac-5bc6-40a4-aea1-bcaf7227fcd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The consequences of this are that a greater volume of blood reenters the pulmonary circulation, the left atria, and the left ventricle. Consequently the compartments of the left heart can eventually fail through volume overload. When the left heart fails, the shunt through the PDA can be reversed, and desaturated blood destined for the pulmonary circulation can end up passing through the PDA to the aorta instead—this reversal later in life is called Eisenmenger syndrome. In Eisenmenger’s the upper extremities receive uncontaminated, saturated blood, as their branching arteries are upstream of the desaturated blood entering the aorta at the PDA. Not so for the lower extremities whose arteries branch after the PDA and so receive low oxygen blood. Hence in Eisenmenger syndrome patients, only the feet are cyanosed.",True,Patent Ductus Arteriosus,,,,
00e57e7b-e776-4cc1-b60b-b537204a1725,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,Atrioventricular Canal,False,Atrioventricular Canal,,,,
39c7c1f7-0837-4d97-bc07-0d2d35eb4ba4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
39c7c1f7-0837-4d97-bc07-0d2d35eb4ba4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
39c7c1f7-0837-4d97-bc07-0d2d35eb4ba4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
39c7c1f7-0837-4d97-bc07-0d2d35eb4ba4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
39c7c1f7-0837-4d97-bc07-0d2d35eb4ba4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
39c7c1f7-0837-4d97-bc07-0d2d35eb4ba4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
39c7c1f7-0837-4d97-bc07-0d2d35eb4ba4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
39c7c1f7-0837-4d97-bc07-0d2d35eb4ba4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
39c7c1f7-0837-4d97-bc07-0d2d35eb4ba4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
34afa493-e572-427b-a4e6-612dc1d0ebad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The malformed valves allow regurgitation, and the unrestricted interventricular communication allow a profound left–right shunt. This leads to volume overload in the pulmonary circulation, and heart failure will be produced if there is no correction. Pulmonary artery hypertension (PAH) and premature development of pulmonary vascular obstructive disease are other common outcomes.",True,Atrioventricular Canal,,,,
a0ca5a79-ee2a-4730-bf5b-2c969031806d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,Truncus Arteriosus,False,Truncus Arteriosus,,,,
66061bca-6ff2-40ea-a038-28cebfa2b5f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
66061bca-6ff2-40ea-a038-28cebfa2b5f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
66061bca-6ff2-40ea-a038-28cebfa2b5f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
66061bca-6ff2-40ea-a038-28cebfa2b5f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
66061bca-6ff2-40ea-a038-28cebfa2b5f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
66061bca-6ff2-40ea-a038-28cebfa2b5f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
66061bca-6ff2-40ea-a038-28cebfa2b5f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
66061bca-6ff2-40ea-a038-28cebfa2b5f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
66061bca-6ff2-40ea-a038-28cebfa2b5f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
d093140c-c134-482f-b2fa-ea089bb1bb58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"The underlying issues with TA are 1) mixing of blood from the left (saturated) and right heart (unsaturated), and 2) the common valve can allow regurgitation. In utero the high pulmonary vascular resistance means most blood exiting the heart goes through the aorta and cardiac output is rarely affected. At birth mild cyanosis can be produced by the mixing of blood from the left and right heart, but as pulmonary vascular resistance remains high in the first few days of life, cardiac output my be maintained. As pulmonary vascular resistance continues to fall in the first few weeks of life, a significant left–right shunt can become established as more left ventricular blood finds it “easier” to ascend up the pulmonary artery. Similar to a VSD, this leads to volume overload in the pulmonary circulation and eventually heart failure. The heart failure has a more rapid onset in TA than VSD if the common valve allows regurgitation. The regurgitation lowers end-diastolic ventricular volumes, so cardiac work to maintain cardiac output increases and promotes myocardial ischemia. Add to this the left–right shunt (as seen in VSD) and heart failure is more likely.",True,Truncus Arteriosus,,,,
414ed42e-072b-459f-8039-62273bbf0221,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,Text,False,Text,,,,
9c7188b7-705e-4565-8231-907fb8b8f0d8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Bhansali, Suneet, and Colin Phoon. Truncus Arteriosis. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK534774/, CC BY 4.0.",True,Text,,,,
5ae83f3c-59ba-4ea2-b226-4ad1d9c8ca20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Cunningham, Jonathan W., and David W. Brown. “Congenital Heart Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, edited by Leonard S. Lilly, Chapter 16. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2012.",True,Text,,,,
a38bfcf0-1f85-42cc-b6d6-adee1ffdfbc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Dakkak, Wael, and Tony I. Oliver. Ventricular Septal Defect. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK470330/, CC BY 4.0.",True,Text,,,,
00784209-370f-4293-98ed-d81108a55864,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Diaz-Frias, Josua, and Melissa Guillaume. Tetralogy of Fallot. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK513288/, CC BY 4.0.",True,Text,,,,
92850419-36d9-4041-bc7e-eafc5537c5b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Gillam-Krakauer, Maria, and Kunal Mahajan. Patent Ductus Ateriosus. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430758/, CC BY 4.0.",True,Text,,,,
ae2600a9-506b-493b-a3ec-e7b3814c281f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Law, Mark A., and Vijai  S. Tivakaran. Coarctation of the Aorta. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430913/, CC BY 4.0.",True,Text,,,,
ee36b0a1-310c-4430-929d-0a46ff6a0b51,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Menillo, Alexandra M., Lawrence S. Lee, and Anthony L. Pearson-Shaver. Atrial Septal Defect. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK535440/, CC BY 4.0.",True,Text,,,,
5a59c58a-3f39-4132-9297-a66b019871fd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Szymanski, Michael W., Sheila M. Moore, Stacy M. Kritzmire, and Amandeep Goyal. Transposition of the Great Arteries. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430758/, CC BY 4.0.",True,Text,,,,
93f1d038-8d11-4ad2-98dc-716721777176,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/#chapter-40-section-1,"Umapathi, Krishna Kishore, and Pradyumna Agasthi. Atrioventricular Canal Defects. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK557511/, CC BY 4.0.",True,Text,,,,
db853774-c70f-42e9-955a-394fc0daf198,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,Embryology,False,Embryology,,,,
fff5bd21-5454-4806-9ac0-d5236fa9ec01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,The most common atrial septal defects arise from:,False,The most common atrial septal defects arise from:,,,,
12c0a1cb-817a-4856-889b-0aca076c61d4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"A patent foramen ovale (20 percent of the population) is not a true ASD as no tissue is missing and the remaining tissue acts as a one-way valve, so a PFO does not have the same pathophysiology as a true ASD. ASDs are common in infants with Down syndrome, as are VSDs.",True,The most common atrial septal defects arise from:,,,,
a11b7e3e-e245-4cf7-8722-e69933e10fc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,Pathophysiology,False,Pathophysiology,,,,
628df991-c167-457d-bc13-7dc555329020,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
628df991-c167-457d-bc13-7dc555329020,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
628df991-c167-457d-bc13-7dc555329020,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
628df991-c167-457d-bc13-7dc555329020,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
628df991-c167-457d-bc13-7dc555329020,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
628df991-c167-457d-bc13-7dc555329020,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
628df991-c167-457d-bc13-7dc555329020,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
628df991-c167-457d-bc13-7dc555329020,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
628df991-c167-457d-bc13-7dc555329020,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"ASDs allow blood flow between the atria. As the pressure in the left atria is higher than that in the left, blood flows from left to right (figure 6.1). This causes volume overload of the right side of the heart. This excessive load may lead to right ventricular compliance being reduced as remodeling takes place. The reduced compliance can elevate right-side pressure and thereby reduce the left–right shunt.",True,Pathophysiology,Figure 6.1,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.1.png,Figure 6.1: Schematic of ASD showing left–right shunt. Thicker lines indicate the presence of volume overload.
ec261069-b546-4445-91fa-98e53d37946b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,Ventricular Septal Defect (VSD),False,Ventricular Septal Defect (VSD),,,,
01d52b79-d030-42f2-9bcd-d67884de4084,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Most ventricular septal defects arise from membraneous portion of the septum (70 percent), while others form in the muscular portion (20 percent); less frequently they occur near the aortic or AV valves.",True,Ventricular Septal Defect (VSD),,,,
0c333eaa-5d49-4773-a0e9-c4d941a226f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
0c333eaa-5d49-4773-a0e9-c4d941a226f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
0c333eaa-5d49-4773-a0e9-c4d941a226f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
0c333eaa-5d49-4773-a0e9-c4d941a226f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
0c333eaa-5d49-4773-a0e9-c4d941a226f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
0c333eaa-5d49-4773-a0e9-c4d941a226f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
0c333eaa-5d49-4773-a0e9-c4d941a226f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
0c333eaa-5d49-4773-a0e9-c4d941a226f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
0c333eaa-5d49-4773-a0e9-c4d941a226f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The manifestations of a VSD depend on the VSD size and the relative resistance of the pulmonary and systemic circulations—all of which will determine the direction of blood flow. During fetal development, the pulmonary and systemic circulations have equivalent resistances, so there may be very little shunting through the VSD, particularly if it is small. After birth, however, the resistance of the pulmonary system falls dramatically, so right ventricular pressure is lower and below left ventricular pressure (which still has to contend with systemic resistance)—consequently a left–right shunt is established. If this shunt is large (depending on the size of the defect), then blood returning from the pulmonary circulation to the left atrium can pass into the left ventricle, through the VSD into the right ventricle and head back into pulmonary circulation to start this loop again (figure 6.2).",True,Ventricular Septal Defect (VSD),Figure 6.2,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
43ebaee6-e512-47b0-aa9e-dc843cd64fd7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
43ebaee6-e512-47b0-aa9e-dc843cd64fd7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
43ebaee6-e512-47b0-aa9e-dc843cd64fd7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
43ebaee6-e512-47b0-aa9e-dc843cd64fd7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
43ebaee6-e512-47b0-aa9e-dc843cd64fd7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
43ebaee6-e512-47b0-aa9e-dc843cd64fd7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
43ebaee6-e512-47b0-aa9e-dc843cd64fd7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
43ebaee6-e512-47b0-aa9e-dc843cd64fd7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
43ebaee6-e512-47b0-aa9e-dc843cd64fd7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"When a large VSD is present, the recirculated blood causes volume overload of the right ventricle and the pulmonary circulation and subsequently both chambers of the left heart (figure 6.2). This can eventually cause chamber dilation and lead to heart failure. The extra volume load in the pulmonary circulation can also lead to early onset of pulmonary vascular disease.",True,Ventricular Septal Defect (VSD),Figure 6.2,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.2.png,"Figure 6.2: Schematic of VSD showing left–right shunt that can lead to volume overload in the RV, LA, LV, and pulmonary circulation. Dotted lines show the recirculation of blood back through the pulmonary circulation. Thicker lines denote volume overload."
8153b8c6-6f54-4144-8bd9-bb886bbda3f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,Coarctation of the Aorta,False,Coarctation of the Aorta,,,,
b809a483-ab25-422f-a505-059c90797e57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
b809a483-ab25-422f-a505-059c90797e57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
b809a483-ab25-422f-a505-059c90797e57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
b809a483-ab25-422f-a505-059c90797e57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
b809a483-ab25-422f-a505-059c90797e57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
b809a483-ab25-422f-a505-059c90797e57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
b809a483-ab25-422f-a505-059c90797e57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
b809a483-ab25-422f-a505-059c90797e57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
b809a483-ab25-422f-a505-059c90797e57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Coarctation of the aorta (figure 6.3) is a constriction of the aortic lumen, usually close to the ductus. The cause is unclear, but low flow through the left heart and aorta flow during development may cause the defect (no flow, no grow).",True,Coarctation of the Aorta,Figure 6.3,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.3-scaled.jpg,Figure 6.3: Coarctation of the aorta (circled).
b111b368-d6c6-4fa7-b611-9456b91545b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The diminished lumen causes increased afterload on the left ventricle. Vessels branching off the aorta before the coarctation can receive normal blood flow, so the head (carotid) and upper extremities (subclavian) are usually properly perfused whereas branching arteries after the coarctation may be underperfused. Consequently, differential cyanosis is a possible manifestation.",True,Coarctation of the Aorta,,,,
b5321672-69cc-42d4-b304-1b59e8fb755a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,Tetralogy of Fallot (ToF),False,Tetralogy of Fallot (ToF),,,,
479bc179-5c5f-4758-af37-7e80ea886f75,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,In Tetralogy of Fallot (ToF) the outflow tract (infundibular) portion of the interventricular septum is displaced. This single defect leads to four defects:,True,Tetralogy of Fallot (ToF),,,,
61e3dce9-7b3c-442c-bed9-8b5ae2b9d057,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Other defects can be associated with ToF, but the defects listed above lead this to be the most common form of cyanotic congenital heart disease.",True,Tetralogy of Fallot (ToF),,,,
698675ef-1a50-4301-a77d-7694537bd8e0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
698675ef-1a50-4301-a77d-7694537bd8e0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
698675ef-1a50-4301-a77d-7694537bd8e0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
698675ef-1a50-4301-a77d-7694537bd8e0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
698675ef-1a50-4301-a77d-7694537bd8e0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
698675ef-1a50-4301-a77d-7694537bd8e0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
698675ef-1a50-4301-a77d-7694537bd8e0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
698675ef-1a50-4301-a77d-7694537bd8e0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
698675ef-1a50-4301-a77d-7694537bd8e0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The high resistance of the stenosed pulmonic valve (#1, figure 6.4) causes the blood in the right ventricle to exit through VSD (#3, figure 6.4) and enter the left ventricle forming a right-left shunt, bypassing the pulmonary circulation. Consequently blood with venous PO2 enters the systemic circulation and hypoxemia/cyanosis results. The degree of hypoxemia/cyanosis that occurs depends on the degree of pulmonic stenosis.",True,Tetralogy of Fallot (ToF),Figure 6.4,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.4-new-scaled.jpg,"Figure 6.4: Tetralogy of Fallot with 1) pulmonic stenosis, 2) RV hypertrophy, 3) VSD, and 4) overriding aorta."
40acdae8-96fb-4c8c-a246-810854f56bb0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,Transposition of the Great Arteries,False,Transposition of the Great Arteries,,,,
3677c4e9-6bb3-4a39-8a7b-9d8d1a16bb13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Although not completely understood, it is thought that failure of the aortic-pulmonary septum to spiral during development results in the great vessels coming off the wrong ventricles—the aorta exits the right, and the pulmonary artery exits the left. Other theories exist.",True,Transposition of the Great Arteries,,,,
8034ffac-e213-471f-b323-b17d5346b597,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
8034ffac-e213-471f-b323-b17d5346b597,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
8034ffac-e213-471f-b323-b17d5346b597,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
8034ffac-e213-471f-b323-b17d5346b597,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
8034ffac-e213-471f-b323-b17d5346b597,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
8034ffac-e213-471f-b323-b17d5346b597,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
8034ffac-e213-471f-b323-b17d5346b597,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
8034ffac-e213-471f-b323-b17d5346b597,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
8034ffac-e213-471f-b323-b17d5346b597,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The placement of the pulmonary artery on the left means left ventricular blood is pumped up to pulmonary circulation, only to return to the left side of the heart via the pulmonary veins. Similarly, the aorta on the right forms a closed-system with the right ventricle pumping into the systemic circulation, only for it to return to the right atrium via the vena cava (see figure 6.5). So how is this compatible with life? In short, it is not. Embryonic development can continue because the two looped circulations can mix at the ductus arteriosus and foramen ovale of the fetal circulation. But after birth these shunts between the two circulations MUST be artificially maintained, or the patient must be “fortunate” enough to also have a VSD for mixing to take place.",True,Transposition of the Great Arteries,Figure 6.5,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.5.png,"Figure 6.5: Schematic of transposition of the great vessels (aorta off of the right, pulmonary artery off of the left) forming two separate, looped circulations."
3b73e0e8-1e18-468f-8758-066331a3e794,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,Patent Ductus Arteriosus,False,Patent Ductus Arteriosus,,,,
24fbb78b-2901-43b7-880f-0c168a9a2538,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The ductus arteriosus is part of the fetal circulation allowing blood in the pulmonary artery to bypass the nonfunctional, high resistance lungs and instead traverse into the aorta and systemic circulation. The ductus should close at birth, and failure to do so leaves a patent ductus arteriosus (PDA).",True,Patent Ductus Arteriosus,,,,
732ea9e2-ec28-4687-96d6-71fa135df9e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
732ea9e2-ec28-4687-96d6-71fa135df9e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
732ea9e2-ec28-4687-96d6-71fa135df9e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
732ea9e2-ec28-4687-96d6-71fa135df9e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
732ea9e2-ec28-4687-96d6-71fa135df9e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
732ea9e2-ec28-4687-96d6-71fa135df9e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
732ea9e2-ec28-4687-96d6-71fa135df9e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
732ea9e2-ec28-4687-96d6-71fa135df9e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
732ea9e2-ec28-4687-96d6-71fa135df9e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"In utero, the high resistance of the pulmonary circulation ensures that blood is diverted through the ductus arteriosis into the aorta. However, at birth there is a dramatic fall in the resistance of the pulmonary circulation as the lungs inflate. The pressure gradient across the ductus is consequently reversed (low on the pulmonary side, high on the systemic), so if the ductus remains open blood will flow from the aorta to the pulmonary artery (i.e., the opposite direction to fetal circulation) (figure 6.6).",True,Patent Ductus Arteriosus,Figure 6.6,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.6.png,Figure 6.6: Schematic of PDA with flow from the aorta to the pulmonary artery. Thicker lines denote volume overload.
a37c9318-e7b0-40b7-ba17-4c883bb52944,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The consequences of this are that a greater volume of blood reenters the pulmonary circulation, the left atria, and the left ventricle. Consequently the compartments of the left heart can eventually fail through volume overload. When the left heart fails, the shunt through the PDA can be reversed, and desaturated blood destined for the pulmonary circulation can end up passing through the PDA to the aorta instead—this reversal later in life is called Eisenmenger syndrome. In Eisenmenger’s the upper extremities receive uncontaminated, saturated blood, as their branching arteries are upstream of the desaturated blood entering the aorta at the PDA. Not so for the lower extremities whose arteries branch after the PDA and so receive low oxygen blood. Hence in Eisenmenger syndrome patients, only the feet are cyanosed.",True,Patent Ductus Arteriosus,,,,
74bc8278-23b7-4b29-a442-2913fc7f73ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,Atrioventricular Canal,False,Atrioventricular Canal,,,,
b788c18d-7611-4c21-9594-d1d0d8e7d996,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
b788c18d-7611-4c21-9594-d1d0d8e7d996,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
b788c18d-7611-4c21-9594-d1d0d8e7d996,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
b788c18d-7611-4c21-9594-d1d0d8e7d996,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
b788c18d-7611-4c21-9594-d1d0d8e7d996,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
b788c18d-7611-4c21-9594-d1d0d8e7d996,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
b788c18d-7611-4c21-9594-d1d0d8e7d996,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
b788c18d-7611-4c21-9594-d1d0d8e7d996,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
b788c18d-7611-4c21-9594-d1d0d8e7d996,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Complete AV canal defect is a result of complete failure of fusion between endocardial cushions. It is characterized by a primum atrial septal defect (#1, figure 6.7) that is contiguous with a ventricular septal defect (#4 in figure 6.7) and a malformed or common AV valve. Although several forms of this defect exist, this complete form is effectively a single chambered heart.",True,Atrioventricular Canal,Figure 6.7,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.7.png,"Figure 6.7: AV Canal with 1) ASD, 2&3) AV valve defects, and 4) VSD."
38b94f56-223b-40ef-b1b0-bdcbffe601fd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The malformed valves allow regurgitation, and the unrestricted interventricular communication allow a profound left–right shunt. This leads to volume overload in the pulmonary circulation, and heart failure will be produced if there is no correction. Pulmonary artery hypertension (PAH) and premature development of pulmonary vascular obstructive disease are other common outcomes.",True,Atrioventricular Canal,,,,
2fdd0dea-484c-4583-bd6e-819f066d73a3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,Truncus Arteriosus,False,Truncus Arteriosus,,,,
617b7427-112e-405e-820d-5cb8b147bb04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Truncus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
617b7427-112e-405e-820d-5cb8b147bb04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Atrioventricular Canal,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
617b7427-112e-405e-820d-5cb8b147bb04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Patent Ductus Arteriosus,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
617b7427-112e-405e-820d-5cb8b147bb04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Transposition of the Great Arteries,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
617b7427-112e-405e-820d-5cb8b147bb04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Tetralogy of Fallot (ToF),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
617b7427-112e-405e-820d-5cb8b147bb04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Coarctation of the Aorta,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
617b7427-112e-405e-820d-5cb8b147bb04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Ventricular Septal Defect (VSD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
617b7427-112e-405e-820d-5cb8b147bb04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,Atrial Septal Defect (ASD),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
617b7427-112e-405e-820d-5cb8b147bb04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,Failed development of the truncoconal septum that normally leads to separation of the pulmonary artery and aorta leads to truncus arteriosus (TA). This condition leads to a single vessel with a single (often incompetent) valve positioned above the ventricular septum (see figure 6.8).,True,Truncus Arteriosus,Figure 6.8,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/6.8-copy.png,Figure 6.8: Truncus arteriosus.
c5f57911-43d6-4ace-8f9c-f2b9f1c9d610,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"The underlying issues with TA are 1) mixing of blood from the left (saturated) and right heart (unsaturated), and 2) the common valve can allow regurgitation. In utero the high pulmonary vascular resistance means most blood exiting the heart goes through the aorta and cardiac output is rarely affected. At birth mild cyanosis can be produced by the mixing of blood from the left and right heart, but as pulmonary vascular resistance remains high in the first few days of life, cardiac output my be maintained. As pulmonary vascular resistance continues to fall in the first few weeks of life, a significant left–right shunt can become established as more left ventricular blood finds it “easier” to ascend up the pulmonary artery. Similar to a VSD, this leads to volume overload in the pulmonary circulation and eventually heart failure. The heart failure has a more rapid onset in TA than VSD if the common valve allows regurgitation. The regurgitation lowers end-diastolic ventricular volumes, so cardiac work to maintain cardiac output increases and promotes myocardial ischemia. Add to this the left–right shunt (as seen in VSD) and heart failure is more likely.",True,Truncus Arteriosus,,,,
d99039a8-bf65-4751-af13-362ec8649e2e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,Text,False,Text,,,,
7212bcc8-7b40-4940-9cae-f15b78197382,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Bhansali, Suneet, and Colin Phoon. Truncus Arteriosis. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK534774/, CC BY 4.0.",True,Text,,,,
14988b29-d9e9-44b3-a755-a26852a6b7f3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Cunningham, Jonathan W., and David W. Brown. “Congenital Heart Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, edited by Leonard S. Lilly, Chapter 16. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2012.",True,Text,,,,
0d14ac62-d349-4308-9646-25c7b4850e05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Dakkak, Wael, and Tony I. Oliver. Ventricular Septal Defect. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK470330/, CC BY 4.0.",True,Text,,,,
43db6ea7-7e1c-417a-a413-1a347b9905fd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Diaz-Frias, Josua, and Melissa Guillaume. Tetralogy of Fallot. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK513288/, CC BY 4.0.",True,Text,,,,
fcd7a998-c894-4e69-ab51-17d1a29cb3b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Gillam-Krakauer, Maria, and Kunal Mahajan. Patent Ductus Ateriosus. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430758/, CC BY 4.0.",True,Text,,,,
0d7beb1f-fee6-4b75-8c10-bcfed371884c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Law, Mark A., and Vijai  S. Tivakaran. Coarctation of the Aorta. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430913/, CC BY 4.0.",True,Text,,,,
7af1b5d2-84cf-4cd6-9617-85bfc61d5726,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Menillo, Alexandra M., Lawrence S. Lee, and Anthony L. Pearson-Shaver. Atrial Septal Defect. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK535440/, CC BY 4.0.",True,Text,,,,
283c90a2-a271-438f-b854-ce8f8cbbcdfc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Szymanski, Michael W., Sheila M. Moore, Stacy M. Kritzmire, and Amandeep Goyal. Transposition of the Great Arteries. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430758/, CC BY 4.0.",True,Text,,,,
acc3c083-4a10-401a-925c-cc6ee26f138b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,6. Congenital Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-6-congenital-heart-disease/,"Umapathi, Krishna Kishore, and Pradyumna Agasthi. Atrioventricular Canal Defects. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK557511/, CC BY 4.0.",True,Text,,,,
d8d591c3-619a-4016-9b13-b8fdb39f286b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,unintrusive,False,unintrusive,,,,
5ffbc2bb-1935-4280-878f-182fffd98c9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,The first and second sounds (S1 and S2) are the fundamental heart sounds.,True,unintrusive,,,,
334f25ea-7306-46ac-9e69-58e46df94d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"S1 occurs at the beginning of isovolumetric contraction. The ventricle is beginning to contract, so ventricular pressure quickly rises above atrial pressure and the atrioventricular (tricuspid and mitral) valves close, producing the S1 sound. The mitral valve normally closes slightly (0.04 seconds) before the tricuspid, causing S1 to be “split” (i.e., actually being two sounds, M1 and T1 (figure 5.1)), but the time gap is too short with a normal heart to be detectable with a stethoscope. The reasons for M1 preceding T1 are not clear, but may be due to the force generation of the left ventricle being slightly faster than that of the right ventricle. The splitting of S1 can be more pronounced and audible in the presence of a right bundle branch block (figure 5.1) that causes left ventricular contraction (and mitral valve closure) to markedly precede contraction of the right ventricle. Conversely, in the case of a left bundle branch block, the normal splitting of S1 may be absent (figure 5.1) as M1 is delayed and so occurs in synchrony with T1.",True,unintrusive,Figure 5.1,Heart Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
334f25ea-7306-46ac-9e69-58e46df94d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"S1 occurs at the beginning of isovolumetric contraction. The ventricle is beginning to contract, so ventricular pressure quickly rises above atrial pressure and the atrioventricular (tricuspid and mitral) valves close, producing the S1 sound. The mitral valve normally closes slightly (0.04 seconds) before the tricuspid, causing S1 to be “split” (i.e., actually being two sounds, M1 and T1 (figure 5.1)), but the time gap is too short with a normal heart to be detectable with a stethoscope. The reasons for M1 preceding T1 are not clear, but may be due to the force generation of the left ventricle being slightly faster than that of the right ventricle. The splitting of S1 can be more pronounced and audible in the presence of a right bundle branch block (figure 5.1) that causes left ventricular contraction (and mitral valve closure) to markedly precede contraction of the right ventricle. Conversely, in the case of a left bundle branch block, the normal splitting of S1 may be absent (figure 5.1) as M1 is delayed and so occurs in synchrony with T1.",True,unintrusive,Figure 5.1,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
334f25ea-7306-46ac-9e69-58e46df94d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"S1 occurs at the beginning of isovolumetric contraction. The ventricle is beginning to contract, so ventricular pressure quickly rises above atrial pressure and the atrioventricular (tricuspid and mitral) valves close, producing the S1 sound. The mitral valve normally closes slightly (0.04 seconds) before the tricuspid, causing S1 to be “split” (i.e., actually being two sounds, M1 and T1 (figure 5.1)), but the time gap is too short with a normal heart to be detectable with a stethoscope. The reasons for M1 preceding T1 are not clear, but may be due to the force generation of the left ventricle being slightly faster than that of the right ventricle. The splitting of S1 can be more pronounced and audible in the presence of a right bundle branch block (figure 5.1) that causes left ventricular contraction (and mitral valve closure) to markedly precede contraction of the right ventricle. Conversely, in the case of a left bundle branch block, the normal splitting of S1 may be absent (figure 5.1) as M1 is delayed and so occurs in synchrony with T1.",True,unintrusive,Figure 5.1,Heart Sounds,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
334f25ea-7306-46ac-9e69-58e46df94d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"S1 occurs at the beginning of isovolumetric contraction. The ventricle is beginning to contract, so ventricular pressure quickly rises above atrial pressure and the atrioventricular (tricuspid and mitral) valves close, producing the S1 sound. The mitral valve normally closes slightly (0.04 seconds) before the tricuspid, causing S1 to be “split” (i.e., actually being two sounds, M1 and T1 (figure 5.1)), but the time gap is too short with a normal heart to be detectable with a stethoscope. The reasons for M1 preceding T1 are not clear, but may be due to the force generation of the left ventricle being slightly faster than that of the right ventricle. The splitting of S1 can be more pronounced and audible in the presence of a right bundle branch block (figure 5.1) that causes left ventricular contraction (and mitral valve closure) to markedly precede contraction of the right ventricle. Conversely, in the case of a left bundle branch block, the normal splitting of S1 may be absent (figure 5.1) as M1 is delayed and so occurs in synchrony with T1.",True,unintrusive,Figure 5.1,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
724a9152-0b3a-4764-ba81-4c3120c38cff,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"S2 is caused by closure of the aortic and pulmonic valves at the beginning of isovolumetric ventricular relaxation when ventricular pressure falls below pulmonary and aortic pressure. As aortic pressure (80 mmHg) is far greater than pulmonary artery pressure (10 mmHg), S2 is normally split with two components (A2 and P2) relating to the closure of the aortic and pulmonic valves, respectively. How split A2 and P2 are depend on physiological conditions, primarily the phase of breathing that influences the pulmonary artery pressure. In expiration pulmonary artery pressure is higher, so the pulmonic valve closes earlier and P2 occurs closer to A2. Conversely, during inspiration pulmonary artery pressure falls, so pulmonic valve closing occurs later and A2 and P2 occur further apart (figure 5.2). This physiological splitting can be heard with a stethoscope, but can be further influenced by diseases as listed in table 5.1.",True,unintrusive,Figure 5.2,Heart Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.2-scaled.jpg,Figure 5.2: Normal splitting of S2 with inspiration.
724a9152-0b3a-4764-ba81-4c3120c38cff,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"S2 is caused by closure of the aortic and pulmonic valves at the beginning of isovolumetric ventricular relaxation when ventricular pressure falls below pulmonary and aortic pressure. As aortic pressure (80 mmHg) is far greater than pulmonary artery pressure (10 mmHg), S2 is normally split with two components (A2 and P2) relating to the closure of the aortic and pulmonic valves, respectively. How split A2 and P2 are depend on physiological conditions, primarily the phase of breathing that influences the pulmonary artery pressure. In expiration pulmonary artery pressure is higher, so the pulmonic valve closes earlier and P2 occurs closer to A2. Conversely, during inspiration pulmonary artery pressure falls, so pulmonic valve closing occurs later and A2 and P2 occur further apart (figure 5.2). This physiological splitting can be heard with a stethoscope, but can be further influenced by diseases as listed in table 5.1.",True,unintrusive,Figure 5.2,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.2-scaled.jpg,Figure 5.2: Normal splitting of S2 with inspiration.
724a9152-0b3a-4764-ba81-4c3120c38cff,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"S2 is caused by closure of the aortic and pulmonic valves at the beginning of isovolumetric ventricular relaxation when ventricular pressure falls below pulmonary and aortic pressure. As aortic pressure (80 mmHg) is far greater than pulmonary artery pressure (10 mmHg), S2 is normally split with two components (A2 and P2) relating to the closure of the aortic and pulmonic valves, respectively. How split A2 and P2 are depend on physiological conditions, primarily the phase of breathing that influences the pulmonary artery pressure. In expiration pulmonary artery pressure is higher, so the pulmonic valve closes earlier and P2 occurs closer to A2. Conversely, during inspiration pulmonary artery pressure falls, so pulmonic valve closing occurs later and A2 and P2 occur further apart (figure 5.2). This physiological splitting can be heard with a stethoscope, but can be further influenced by diseases as listed in table 5.1.",True,unintrusive,Figure 5.2,Heart Sounds,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.2-scaled.jpg,Figure 5.2: Normal splitting of S2 with inspiration.
724a9152-0b3a-4764-ba81-4c3120c38cff,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"S2 is caused by closure of the aortic and pulmonic valves at the beginning of isovolumetric ventricular relaxation when ventricular pressure falls below pulmonary and aortic pressure. As aortic pressure (80 mmHg) is far greater than pulmonary artery pressure (10 mmHg), S2 is normally split with two components (A2 and P2) relating to the closure of the aortic and pulmonic valves, respectively. How split A2 and P2 are depend on physiological conditions, primarily the phase of breathing that influences the pulmonary artery pressure. In expiration pulmonary artery pressure is higher, so the pulmonic valve closes earlier and P2 occurs closer to A2. Conversely, during inspiration pulmonary artery pressure falls, so pulmonic valve closing occurs later and A2 and P2 occur further apart (figure 5.2). This physiological splitting can be heard with a stethoscope, but can be further influenced by diseases as listed in table 5.1.",True,unintrusive,Figure 5.2,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.2-scaled.jpg,Figure 5.2: Normal splitting of S2 with inspiration.
4d7c531a-16ee-4653-afbd-f021fd27c395,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,Table 5.1: Changes in S2 splitting and possible underlying causes.,True,unintrusive,,,,
b85a54b0-6aea-444b-b9c5-1b982105fbc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"S3 is associated with the rapid filling phase of the ventricle (when the AV valves open), about 0.14 to 0.16 seconds after S2 (closure of the aortic and pulmonic valves). The exact cause of the sound is unclear, but a normal S3 occurs as a brief, low-frequency vibration. Previously thought to be an intracardiac sound arising from vibrations in the valve cusps or ventricular wall, more recent studies suggest the sound may be due to the filling ventricular wall hitting the inner chest wall, or it may arise from the ventricular apex as it hits a limitation of its longitudinal expansion.",True,unintrusive,,,,
41134bf7-67fa-419e-b65e-355eba0c75ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,Table 5.2: Common causes of abnormal S3.,True,unintrusive,,,,
b6f4bdf6-2cdb-4402-978e-0d2c0f12ef68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"As S3 is a filling sound, an abnormal S3 (higher pitch and referred to as a ventricular gallop) is an important clue to heart failure or volume overload (see table 5.2). The absence of an abnormal S3 does not rule out heart failure, but its presence is a sensitive indicator of ventricular dysfunction. Constriction around the heart (e.g., constrictive pericarditis) may cause an early S3, or “pericardial knock.”",True,unintrusive,,,,
8e78b9d6-934e-48c2-8d8e-2a605bc52c8b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"S4 is abnormal and is associated with poor ventricular compliance (e.g., ventricular hypertrophy). It occurs during atrial contraction and is associated with the atrial pressure pulse. The sound is thought to be caused by reverberation of the stiffened ventricular wall as blood is propelled into the ventricle from the atrium (hence it is also known as an atrial gallop). S4 and raised end-diastolic ventricular pressure (EDVP) commonly occur together as both are caused by poor ventricular compliance, so S4 tends to be associated with conditions that cause pressure overload (see table 5.3).",True,unintrusive,,,,
862d6bb6-963f-4074-bc42-16be655a662e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,Table 5.3: Common causes of abnormal S4.,True,unintrusive,,,,
c8f90997-4325-48ec-9369-c2c8ff8c3cdb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,Ejection Sounds (Clicks),False,Ejection Sounds (Clicks),,,,
1f6b22d4-bf70-4b81-afa4-729a627cdae7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"As S1 and S2 occur during closure of heart valves, pathological conditions can lead to the valves producing a high-frequency “clicking” sound when they open during chamber ejection—hence they can be referred to as ejection sounds and they are pathological.",True,Ejection Sounds (Clicks),,,,
a2f5be91-51f5-4d63-bf3e-f8125ee88346,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"Aortic ejection sounds usually occur 0.12–0.14 seconds after the Q-wave of the ECG (i.e., after ventricular pressure has risen to exceed aortic pressure). Because of its timing, the “click” produced can be misinterpreted as a split S1. The abnormal opening of the aortic valve is usually caused by a deformed but mobile valve leaflet or aortic root dilation that may be caused by the conditions listed in table 5.4.",True,Ejection Sounds (Clicks),,,,
7e8d8d0a-4d81-4e44-982a-bcec6f5b34c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"Pulmonary ejection sounds occur a little earlier (0.09–0.11 seconds) after the Q-wave as the pulmonary valve opens a little earlier (figure 5.1). It can also be distinguished by the fact that its intensity is diminished during inspiration as increased venous return during inspiration augments the effect of atrial contraction and causes a “gentler” opening of the valve. As with the aortic ejection sounds, pulmonary ejection sounds are associated with deformed valves or pulmonary arterial dilation.",True,Ejection Sounds (Clicks),Figure 5.1,Heart Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
7e8d8d0a-4d81-4e44-982a-bcec6f5b34c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"Pulmonary ejection sounds occur a little earlier (0.09–0.11 seconds) after the Q-wave as the pulmonary valve opens a little earlier (figure 5.1). It can also be distinguished by the fact that its intensity is diminished during inspiration as increased venous return during inspiration augments the effect of atrial contraction and causes a “gentler” opening of the valve. As with the aortic ejection sounds, pulmonary ejection sounds are associated with deformed valves or pulmonary arterial dilation.",True,Ejection Sounds (Clicks),Figure 5.1,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
7e8d8d0a-4d81-4e44-982a-bcec6f5b34c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"Pulmonary ejection sounds occur a little earlier (0.09–0.11 seconds) after the Q-wave as the pulmonary valve opens a little earlier (figure 5.1). It can also be distinguished by the fact that its intensity is diminished during inspiration as increased venous return during inspiration augments the effect of atrial contraction and causes a “gentler” opening of the valve. As with the aortic ejection sounds, pulmonary ejection sounds are associated with deformed valves or pulmonary arterial dilation.",True,Ejection Sounds (Clicks),Figure 5.1,Heart Sounds,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
7e8d8d0a-4d81-4e44-982a-bcec6f5b34c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"Pulmonary ejection sounds occur a little earlier (0.09–0.11 seconds) after the Q-wave as the pulmonary valve opens a little earlier (figure 5.1). It can also be distinguished by the fact that its intensity is diminished during inspiration as increased venous return during inspiration augments the effect of atrial contraction and causes a “gentler” opening of the valve. As with the aortic ejection sounds, pulmonary ejection sounds are associated with deformed valves or pulmonary arterial dilation.",True,Ejection Sounds (Clicks),Figure 5.1,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
1b153493-e775-4028-9b43-5efb5d11fad0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"A click occurring in diastole is associated with abnormal opening of either the mitral or tricuspid valve. Similar to systolic clicks, a diastolic click can be misinterpreted as a split S2. The most common cause of diastolic clicks is valvular stenosis of an AV valve.",True,Ejection Sounds (Clicks),,,,
1615eacf-7f87-43a8-b7b5-a3cb428b9d53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"Table 5.4: Common causes of ejection ""clicks.""",True,Ejection Sounds (Clicks),,,,
6d7f8ae7-bcc3-4cd4-b369-87408b0ec793,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,Heart Murmurs,False,Heart Murmurs,,,,
9c3bb02c-fc73-48a6-b44b-aeaa0ac2089e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"A murmur is the sound of turbulence associated with abnormal blood flow through a valve or chamber. The turbulent flow produces low-frequency audible sounds that are distinct from heart sounds associated with valve closures. Murmurs can be divided into those caused by valvular defects and those caused by abnormal interchamber flow. Depending on the defect involved, the murmur may occur during diastole and systole, hence distinguishing whether a murmur is diastolic or systolic is a useful first diagnostic step.",True,Heart Murmurs,,,,
6946a7b2-cc20-4f01-8124-e43277e1447a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"Classification of a murmur includes the intensity (Grades 1–6, faintest to loudest), the pitch (high or low), configuration, location, and timing. The timing refers to the onset and duration of the murmur, and the classifications are shown in table 5.5 with some common causes listed there and below.",True,Heart Murmurs,,,,
4787b84f-230c-41ed-a33c-e809c93db364,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,Table 5.5: Classifications of heart murmurs.,True,Heart Murmurs,,,,
8dc69fad-a1f6-4ec7-8ba4-405ca452b0c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,Text,False,Text,,,,
ade10988-52d5-40bb-a747-06d819e62b55,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"Dornbush, Sean, and Andre E. Turnquest. Physiology, Heart Sounds. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK541010, CC BY 4.0.",True,Text,,,,
1d13203a-5404-4ba4-abaa-6b5f3df36f97,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"Kulkarni, Vivek T., and Leonard S. Lilly. “The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 2. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
3f337c79-9677-4c2d-8bca-e53e383a902f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"Thomas, Seth L., Joseph Heaton, and Amgad N. Makaryus. Physiology, Cardiovascular Murmurs. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK525958, CC BY 4.0.",True,Text,,,,
79ed1809-c439-4208-b3fb-eabdea6a3c5c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-3,"Table 5.5: Classifications of heart murmurs. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/5.5_20220113",True,Text,,,,
48370af8-64f5-499b-82fb-e6cf4ede2f83,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,unintrusive,False,unintrusive,,,,
98045abf-4400-4bc5-92cf-2faccbde2942,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,The first and second sounds (S1 and S2) are the fundamental heart sounds.,True,unintrusive,,,,
8f1f6216-d00a-481e-b79e-cd207c8f1470,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"S1 occurs at the beginning of isovolumetric contraction. The ventricle is beginning to contract, so ventricular pressure quickly rises above atrial pressure and the atrioventricular (tricuspid and mitral) valves close, producing the S1 sound. The mitral valve normally closes slightly (0.04 seconds) before the tricuspid, causing S1 to be “split” (i.e., actually being two sounds, M1 and T1 (figure 5.1)), but the time gap is too short with a normal heart to be detectable with a stethoscope. The reasons for M1 preceding T1 are not clear, but may be due to the force generation of the left ventricle being slightly faster than that of the right ventricle. The splitting of S1 can be more pronounced and audible in the presence of a right bundle branch block (figure 5.1) that causes left ventricular contraction (and mitral valve closure) to markedly precede contraction of the right ventricle. Conversely, in the case of a left bundle branch block, the normal splitting of S1 may be absent (figure 5.1) as M1 is delayed and so occurs in synchrony with T1.",True,unintrusive,Figure 5.1,Heart Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
8f1f6216-d00a-481e-b79e-cd207c8f1470,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"S1 occurs at the beginning of isovolumetric contraction. The ventricle is beginning to contract, so ventricular pressure quickly rises above atrial pressure and the atrioventricular (tricuspid and mitral) valves close, producing the S1 sound. The mitral valve normally closes slightly (0.04 seconds) before the tricuspid, causing S1 to be “split” (i.e., actually being two sounds, M1 and T1 (figure 5.1)), but the time gap is too short with a normal heart to be detectable with a stethoscope. The reasons for M1 preceding T1 are not clear, but may be due to the force generation of the left ventricle being slightly faster than that of the right ventricle. The splitting of S1 can be more pronounced and audible in the presence of a right bundle branch block (figure 5.1) that causes left ventricular contraction (and mitral valve closure) to markedly precede contraction of the right ventricle. Conversely, in the case of a left bundle branch block, the normal splitting of S1 may be absent (figure 5.1) as M1 is delayed and so occurs in synchrony with T1.",True,unintrusive,Figure 5.1,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
8f1f6216-d00a-481e-b79e-cd207c8f1470,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"S1 occurs at the beginning of isovolumetric contraction. The ventricle is beginning to contract, so ventricular pressure quickly rises above atrial pressure and the atrioventricular (tricuspid and mitral) valves close, producing the S1 sound. The mitral valve normally closes slightly (0.04 seconds) before the tricuspid, causing S1 to be “split” (i.e., actually being two sounds, M1 and T1 (figure 5.1)), but the time gap is too short with a normal heart to be detectable with a stethoscope. The reasons for M1 preceding T1 are not clear, but may be due to the force generation of the left ventricle being slightly faster than that of the right ventricle. The splitting of S1 can be more pronounced and audible in the presence of a right bundle branch block (figure 5.1) that causes left ventricular contraction (and mitral valve closure) to markedly precede contraction of the right ventricle. Conversely, in the case of a left bundle branch block, the normal splitting of S1 may be absent (figure 5.1) as M1 is delayed and so occurs in synchrony with T1.",True,unintrusive,Figure 5.1,Heart Sounds,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
8f1f6216-d00a-481e-b79e-cd207c8f1470,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"S1 occurs at the beginning of isovolumetric contraction. The ventricle is beginning to contract, so ventricular pressure quickly rises above atrial pressure and the atrioventricular (tricuspid and mitral) valves close, producing the S1 sound. The mitral valve normally closes slightly (0.04 seconds) before the tricuspid, causing S1 to be “split” (i.e., actually being two sounds, M1 and T1 (figure 5.1)), but the time gap is too short with a normal heart to be detectable with a stethoscope. The reasons for M1 preceding T1 are not clear, but may be due to the force generation of the left ventricle being slightly faster than that of the right ventricle. The splitting of S1 can be more pronounced and audible in the presence of a right bundle branch block (figure 5.1) that causes left ventricular contraction (and mitral valve closure) to markedly precede contraction of the right ventricle. Conversely, in the case of a left bundle branch block, the normal splitting of S1 may be absent (figure 5.1) as M1 is delayed and so occurs in synchrony with T1.",True,unintrusive,Figure 5.1,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
1b8c5004-d7d8-4ae3-9449-09dad9aaf413,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"S2 is caused by closure of the aortic and pulmonic valves at the beginning of isovolumetric ventricular relaxation when ventricular pressure falls below pulmonary and aortic pressure. As aortic pressure (80 mmHg) is far greater than pulmonary artery pressure (10 mmHg), S2 is normally split with two components (A2 and P2) relating to the closure of the aortic and pulmonic valves, respectively. How split A2 and P2 are depend on physiological conditions, primarily the phase of breathing that influences the pulmonary artery pressure. In expiration pulmonary artery pressure is higher, so the pulmonic valve closes earlier and P2 occurs closer to A2. Conversely, during inspiration pulmonary artery pressure falls, so pulmonic valve closing occurs later and A2 and P2 occur further apart (figure 5.2). This physiological splitting can be heard with a stethoscope, but can be further influenced by diseases as listed in table 5.1.",True,unintrusive,Figure 5.2,Heart Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.2-scaled.jpg,Figure 5.2: Normal splitting of S2 with inspiration.
1b8c5004-d7d8-4ae3-9449-09dad9aaf413,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"S2 is caused by closure of the aortic and pulmonic valves at the beginning of isovolumetric ventricular relaxation when ventricular pressure falls below pulmonary and aortic pressure. As aortic pressure (80 mmHg) is far greater than pulmonary artery pressure (10 mmHg), S2 is normally split with two components (A2 and P2) relating to the closure of the aortic and pulmonic valves, respectively. How split A2 and P2 are depend on physiological conditions, primarily the phase of breathing that influences the pulmonary artery pressure. In expiration pulmonary artery pressure is higher, so the pulmonic valve closes earlier and P2 occurs closer to A2. Conversely, during inspiration pulmonary artery pressure falls, so pulmonic valve closing occurs later and A2 and P2 occur further apart (figure 5.2). This physiological splitting can be heard with a stethoscope, but can be further influenced by diseases as listed in table 5.1.",True,unintrusive,Figure 5.2,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.2-scaled.jpg,Figure 5.2: Normal splitting of S2 with inspiration.
1b8c5004-d7d8-4ae3-9449-09dad9aaf413,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"S2 is caused by closure of the aortic and pulmonic valves at the beginning of isovolumetric ventricular relaxation when ventricular pressure falls below pulmonary and aortic pressure. As aortic pressure (80 mmHg) is far greater than pulmonary artery pressure (10 mmHg), S2 is normally split with two components (A2 and P2) relating to the closure of the aortic and pulmonic valves, respectively. How split A2 and P2 are depend on physiological conditions, primarily the phase of breathing that influences the pulmonary artery pressure. In expiration pulmonary artery pressure is higher, so the pulmonic valve closes earlier and P2 occurs closer to A2. Conversely, during inspiration pulmonary artery pressure falls, so pulmonic valve closing occurs later and A2 and P2 occur further apart (figure 5.2). This physiological splitting can be heard with a stethoscope, but can be further influenced by diseases as listed in table 5.1.",True,unintrusive,Figure 5.2,Heart Sounds,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.2-scaled.jpg,Figure 5.2: Normal splitting of S2 with inspiration.
1b8c5004-d7d8-4ae3-9449-09dad9aaf413,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"S2 is caused by closure of the aortic and pulmonic valves at the beginning of isovolumetric ventricular relaxation when ventricular pressure falls below pulmonary and aortic pressure. As aortic pressure (80 mmHg) is far greater than pulmonary artery pressure (10 mmHg), S2 is normally split with two components (A2 and P2) relating to the closure of the aortic and pulmonic valves, respectively. How split A2 and P2 are depend on physiological conditions, primarily the phase of breathing that influences the pulmonary artery pressure. In expiration pulmonary artery pressure is higher, so the pulmonic valve closes earlier and P2 occurs closer to A2. Conversely, during inspiration pulmonary artery pressure falls, so pulmonic valve closing occurs later and A2 and P2 occur further apart (figure 5.2). This physiological splitting can be heard with a stethoscope, but can be further influenced by diseases as listed in table 5.1.",True,unintrusive,Figure 5.2,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.2-scaled.jpg,Figure 5.2: Normal splitting of S2 with inspiration.
bc8b2133-3e03-4374-91e7-f1717bf051b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,Table 5.1: Changes in S2 splitting and possible underlying causes.,True,unintrusive,,,,
d5f5ae1f-261d-4a2c-ae2e-5d18f57e66af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"S3 is associated with the rapid filling phase of the ventricle (when the AV valves open), about 0.14 to 0.16 seconds after S2 (closure of the aortic and pulmonic valves). The exact cause of the sound is unclear, but a normal S3 occurs as a brief, low-frequency vibration. Previously thought to be an intracardiac sound arising from vibrations in the valve cusps or ventricular wall, more recent studies suggest the sound may be due to the filling ventricular wall hitting the inner chest wall, or it may arise from the ventricular apex as it hits a limitation of its longitudinal expansion.",True,unintrusive,,,,
44a1a2ab-e55e-4a1e-bf45-c8fa0a10d236,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,Table 5.2: Common causes of abnormal S3.,True,unintrusive,,,,
31b8e7d9-01ce-49b8-81b1-90af57a2c321,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"As S3 is a filling sound, an abnormal S3 (higher pitch and referred to as a ventricular gallop) is an important clue to heart failure or volume overload (see table 5.2). The absence of an abnormal S3 does not rule out heart failure, but its presence is a sensitive indicator of ventricular dysfunction. Constriction around the heart (e.g., constrictive pericarditis) may cause an early S3, or “pericardial knock.”",True,unintrusive,,,,
6b902a04-a9d9-49c3-93d4-c396eada0527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"S4 is abnormal and is associated with poor ventricular compliance (e.g., ventricular hypertrophy). It occurs during atrial contraction and is associated with the atrial pressure pulse. The sound is thought to be caused by reverberation of the stiffened ventricular wall as blood is propelled into the ventricle from the atrium (hence it is also known as an atrial gallop). S4 and raised end-diastolic ventricular pressure (EDVP) commonly occur together as both are caused by poor ventricular compliance, so S4 tends to be associated with conditions that cause pressure overload (see table 5.3).",True,unintrusive,,,,
b731eace-d8e6-4e79-ac20-c352df5c7b69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,Table 5.3: Common causes of abnormal S4.,True,unintrusive,,,,
d0373ace-05d4-4786-a8de-f0cc246b7c9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,Ejection Sounds (Clicks),False,Ejection Sounds (Clicks),,,,
ef69fe60-1735-4da7-b878-a0bebd8f155f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"As S1 and S2 occur during closure of heart valves, pathological conditions can lead to the valves producing a high-frequency “clicking” sound when they open during chamber ejection—hence they can be referred to as ejection sounds and they are pathological.",True,Ejection Sounds (Clicks),,,,
17ab8743-6eff-4d40-ac92-522c37ea1556,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"Aortic ejection sounds usually occur 0.12–0.14 seconds after the Q-wave of the ECG (i.e., after ventricular pressure has risen to exceed aortic pressure). Because of its timing, the “click” produced can be misinterpreted as a split S1. The abnormal opening of the aortic valve is usually caused by a deformed but mobile valve leaflet or aortic root dilation that may be caused by the conditions listed in table 5.4.",True,Ejection Sounds (Clicks),,,,
8b62cfc0-5720-4d13-b7c8-9d51d8d2eb18,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"Pulmonary ejection sounds occur a little earlier (0.09–0.11 seconds) after the Q-wave as the pulmonary valve opens a little earlier (figure 5.1). It can also be distinguished by the fact that its intensity is diminished during inspiration as increased venous return during inspiration augments the effect of atrial contraction and causes a “gentler” opening of the valve. As with the aortic ejection sounds, pulmonary ejection sounds are associated with deformed valves or pulmonary arterial dilation.",True,Ejection Sounds (Clicks),Figure 5.1,Heart Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
8b62cfc0-5720-4d13-b7c8-9d51d8d2eb18,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"Pulmonary ejection sounds occur a little earlier (0.09–0.11 seconds) after the Q-wave as the pulmonary valve opens a little earlier (figure 5.1). It can also be distinguished by the fact that its intensity is diminished during inspiration as increased venous return during inspiration augments the effect of atrial contraction and causes a “gentler” opening of the valve. As with the aortic ejection sounds, pulmonary ejection sounds are associated with deformed valves or pulmonary arterial dilation.",True,Ejection Sounds (Clicks),Figure 5.1,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
8b62cfc0-5720-4d13-b7c8-9d51d8d2eb18,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"Pulmonary ejection sounds occur a little earlier (0.09–0.11 seconds) after the Q-wave as the pulmonary valve opens a little earlier (figure 5.1). It can also be distinguished by the fact that its intensity is diminished during inspiration as increased venous return during inspiration augments the effect of atrial contraction and causes a “gentler” opening of the valve. As with the aortic ejection sounds, pulmonary ejection sounds are associated with deformed valves or pulmonary arterial dilation.",True,Ejection Sounds (Clicks),Figure 5.1,Heart Sounds,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
8b62cfc0-5720-4d13-b7c8-9d51d8d2eb18,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"Pulmonary ejection sounds occur a little earlier (0.09–0.11 seconds) after the Q-wave as the pulmonary valve opens a little earlier (figure 5.1). It can also be distinguished by the fact that its intensity is diminished during inspiration as increased venous return during inspiration augments the effect of atrial contraction and causes a “gentler” opening of the valve. As with the aortic ejection sounds, pulmonary ejection sounds are associated with deformed valves or pulmonary arterial dilation.",True,Ejection Sounds (Clicks),Figure 5.1,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
e31295c8-c1b5-495a-9d18-be4bc7199cce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"A click occurring in diastole is associated with abnormal opening of either the mitral or tricuspid valve. Similar to systolic clicks, a diastolic click can be misinterpreted as a split S2. The most common cause of diastolic clicks is valvular stenosis of an AV valve.",True,Ejection Sounds (Clicks),,,,
9bdf6b2e-532b-425a-b73e-2dbb044a95e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"Table 5.4: Common causes of ejection ""clicks.""",True,Ejection Sounds (Clicks),,,,
588d519a-1587-4783-91f4-603bac5f2fee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,Heart Murmurs,False,Heart Murmurs,,,,
61144acd-6507-498b-9f65-68dd3e0ada70,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"A murmur is the sound of turbulence associated with abnormal blood flow through a valve or chamber. The turbulent flow produces low-frequency audible sounds that are distinct from heart sounds associated with valve closures. Murmurs can be divided into those caused by valvular defects and those caused by abnormal interchamber flow. Depending on the defect involved, the murmur may occur during diastole and systole, hence distinguishing whether a murmur is diastolic or systolic is a useful first diagnostic step.",True,Heart Murmurs,,,,
1e346d53-3243-4dfa-ab0a-15259d6a9f2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"Classification of a murmur includes the intensity (Grades 1–6, faintest to loudest), the pitch (high or low), configuration, location, and timing. The timing refers to the onset and duration of the murmur, and the classifications are shown in table 5.5 with some common causes listed there and below.",True,Heart Murmurs,,,,
0bf4bbf6-cf91-426c-8f27-93f4d149d9f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,Table 5.5: Classifications of heart murmurs.,True,Heart Murmurs,,,,
7d2d4236-0214-4005-ad41-7ac83ac7b75f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,Text,False,Text,,,,
9352f384-7520-4525-93cb-5970080c2429,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"Dornbush, Sean, and Andre E. Turnquest. Physiology, Heart Sounds. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK541010, CC BY 4.0.",True,Text,,,,
5e2845de-813e-4899-9f27-302a0ddc448e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"Kulkarni, Vivek T., and Leonard S. Lilly. “The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 2. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
dd19c68d-65ec-4192-a537-2db53f980e6b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"Thomas, Seth L., Joseph Heaton, and Amgad N. Makaryus. Physiology, Cardiovascular Murmurs. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK525958, CC BY 4.0.",True,Text,,,,
bb43f877-a998-4caf-8294-7a3b244786cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-2,"Table 5.5: Classifications of heart murmurs. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/5.5_20220113",True,Text,,,,
672953f1-49b1-4c68-8744-a1e7fe308f7f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,unintrusive,False,unintrusive,,,,
f081d8f6-1d28-4b90-af54-97b2736cecb2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,The first and second sounds (S1 and S2) are the fundamental heart sounds.,True,unintrusive,,,,
39d41989-297b-40f3-9438-a8ef0f7e3224,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"S1 occurs at the beginning of isovolumetric contraction. The ventricle is beginning to contract, so ventricular pressure quickly rises above atrial pressure and the atrioventricular (tricuspid and mitral) valves close, producing the S1 sound. The mitral valve normally closes slightly (0.04 seconds) before the tricuspid, causing S1 to be “split” (i.e., actually being two sounds, M1 and T1 (figure 5.1)), but the time gap is too short with a normal heart to be detectable with a stethoscope. The reasons for M1 preceding T1 are not clear, but may be due to the force generation of the left ventricle being slightly faster than that of the right ventricle. The splitting of S1 can be more pronounced and audible in the presence of a right bundle branch block (figure 5.1) that causes left ventricular contraction (and mitral valve closure) to markedly precede contraction of the right ventricle. Conversely, in the case of a left bundle branch block, the normal splitting of S1 may be absent (figure 5.1) as M1 is delayed and so occurs in synchrony with T1.",True,unintrusive,Figure 5.1,Heart Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
39d41989-297b-40f3-9438-a8ef0f7e3224,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"S1 occurs at the beginning of isovolumetric contraction. The ventricle is beginning to contract, so ventricular pressure quickly rises above atrial pressure and the atrioventricular (tricuspid and mitral) valves close, producing the S1 sound. The mitral valve normally closes slightly (0.04 seconds) before the tricuspid, causing S1 to be “split” (i.e., actually being two sounds, M1 and T1 (figure 5.1)), but the time gap is too short with a normal heart to be detectable with a stethoscope. The reasons for M1 preceding T1 are not clear, but may be due to the force generation of the left ventricle being slightly faster than that of the right ventricle. The splitting of S1 can be more pronounced and audible in the presence of a right bundle branch block (figure 5.1) that causes left ventricular contraction (and mitral valve closure) to markedly precede contraction of the right ventricle. Conversely, in the case of a left bundle branch block, the normal splitting of S1 may be absent (figure 5.1) as M1 is delayed and so occurs in synchrony with T1.",True,unintrusive,Figure 5.1,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
39d41989-297b-40f3-9438-a8ef0f7e3224,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"S1 occurs at the beginning of isovolumetric contraction. The ventricle is beginning to contract, so ventricular pressure quickly rises above atrial pressure and the atrioventricular (tricuspid and mitral) valves close, producing the S1 sound. The mitral valve normally closes slightly (0.04 seconds) before the tricuspid, causing S1 to be “split” (i.e., actually being two sounds, M1 and T1 (figure 5.1)), but the time gap is too short with a normal heart to be detectable with a stethoscope. The reasons for M1 preceding T1 are not clear, but may be due to the force generation of the left ventricle being slightly faster than that of the right ventricle. The splitting of S1 can be more pronounced and audible in the presence of a right bundle branch block (figure 5.1) that causes left ventricular contraction (and mitral valve closure) to markedly precede contraction of the right ventricle. Conversely, in the case of a left bundle branch block, the normal splitting of S1 may be absent (figure 5.1) as M1 is delayed and so occurs in synchrony with T1.",True,unintrusive,Figure 5.1,Heart Sounds,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
39d41989-297b-40f3-9438-a8ef0f7e3224,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"S1 occurs at the beginning of isovolumetric contraction. The ventricle is beginning to contract, so ventricular pressure quickly rises above atrial pressure and the atrioventricular (tricuspid and mitral) valves close, producing the S1 sound. The mitral valve normally closes slightly (0.04 seconds) before the tricuspid, causing S1 to be “split” (i.e., actually being two sounds, M1 and T1 (figure 5.1)), but the time gap is too short with a normal heart to be detectable with a stethoscope. The reasons for M1 preceding T1 are not clear, but may be due to the force generation of the left ventricle being slightly faster than that of the right ventricle. The splitting of S1 can be more pronounced and audible in the presence of a right bundle branch block (figure 5.1) that causes left ventricular contraction (and mitral valve closure) to markedly precede contraction of the right ventricle. Conversely, in the case of a left bundle branch block, the normal splitting of S1 may be absent (figure 5.1) as M1 is delayed and so occurs in synchrony with T1.",True,unintrusive,Figure 5.1,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
d899303e-ea7c-4167-80f9-68aa6a7fbacd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"S2 is caused by closure of the aortic and pulmonic valves at the beginning of isovolumetric ventricular relaxation when ventricular pressure falls below pulmonary and aortic pressure. As aortic pressure (80 mmHg) is far greater than pulmonary artery pressure (10 mmHg), S2 is normally split with two components (A2 and P2) relating to the closure of the aortic and pulmonic valves, respectively. How split A2 and P2 are depend on physiological conditions, primarily the phase of breathing that influences the pulmonary artery pressure. In expiration pulmonary artery pressure is higher, so the pulmonic valve closes earlier and P2 occurs closer to A2. Conversely, during inspiration pulmonary artery pressure falls, so pulmonic valve closing occurs later and A2 and P2 occur further apart (figure 5.2). This physiological splitting can be heard with a stethoscope, but can be further influenced by diseases as listed in table 5.1.",True,unintrusive,Figure 5.2,Heart Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.2-scaled.jpg,Figure 5.2: Normal splitting of S2 with inspiration.
d899303e-ea7c-4167-80f9-68aa6a7fbacd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"S2 is caused by closure of the aortic and pulmonic valves at the beginning of isovolumetric ventricular relaxation when ventricular pressure falls below pulmonary and aortic pressure. As aortic pressure (80 mmHg) is far greater than pulmonary artery pressure (10 mmHg), S2 is normally split with two components (A2 and P2) relating to the closure of the aortic and pulmonic valves, respectively. How split A2 and P2 are depend on physiological conditions, primarily the phase of breathing that influences the pulmonary artery pressure. In expiration pulmonary artery pressure is higher, so the pulmonic valve closes earlier and P2 occurs closer to A2. Conversely, during inspiration pulmonary artery pressure falls, so pulmonic valve closing occurs later and A2 and P2 occur further apart (figure 5.2). This physiological splitting can be heard with a stethoscope, but can be further influenced by diseases as listed in table 5.1.",True,unintrusive,Figure 5.2,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.2-scaled.jpg,Figure 5.2: Normal splitting of S2 with inspiration.
d899303e-ea7c-4167-80f9-68aa6a7fbacd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"S2 is caused by closure of the aortic and pulmonic valves at the beginning of isovolumetric ventricular relaxation when ventricular pressure falls below pulmonary and aortic pressure. As aortic pressure (80 mmHg) is far greater than pulmonary artery pressure (10 mmHg), S2 is normally split with two components (A2 and P2) relating to the closure of the aortic and pulmonic valves, respectively. How split A2 and P2 are depend on physiological conditions, primarily the phase of breathing that influences the pulmonary artery pressure. In expiration pulmonary artery pressure is higher, so the pulmonic valve closes earlier and P2 occurs closer to A2. Conversely, during inspiration pulmonary artery pressure falls, so pulmonic valve closing occurs later and A2 and P2 occur further apart (figure 5.2). This physiological splitting can be heard with a stethoscope, but can be further influenced by diseases as listed in table 5.1.",True,unintrusive,Figure 5.2,Heart Sounds,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.2-scaled.jpg,Figure 5.2: Normal splitting of S2 with inspiration.
d899303e-ea7c-4167-80f9-68aa6a7fbacd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"S2 is caused by closure of the aortic and pulmonic valves at the beginning of isovolumetric ventricular relaxation when ventricular pressure falls below pulmonary and aortic pressure. As aortic pressure (80 mmHg) is far greater than pulmonary artery pressure (10 mmHg), S2 is normally split with two components (A2 and P2) relating to the closure of the aortic and pulmonic valves, respectively. How split A2 and P2 are depend on physiological conditions, primarily the phase of breathing that influences the pulmonary artery pressure. In expiration pulmonary artery pressure is higher, so the pulmonic valve closes earlier and P2 occurs closer to A2. Conversely, during inspiration pulmonary artery pressure falls, so pulmonic valve closing occurs later and A2 and P2 occur further apart (figure 5.2). This physiological splitting can be heard with a stethoscope, but can be further influenced by diseases as listed in table 5.1.",True,unintrusive,Figure 5.2,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.2-scaled.jpg,Figure 5.2: Normal splitting of S2 with inspiration.
b0e3c531-a4e6-4d73-8491-f673bd62637e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,Table 5.1: Changes in S2 splitting and possible underlying causes.,True,unintrusive,,,,
27c0b307-6345-4d41-8b11-acdcb47f2ca6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"S3 is associated with the rapid filling phase of the ventricle (when the AV valves open), about 0.14 to 0.16 seconds after S2 (closure of the aortic and pulmonic valves). The exact cause of the sound is unclear, but a normal S3 occurs as a brief, low-frequency vibration. Previously thought to be an intracardiac sound arising from vibrations in the valve cusps or ventricular wall, more recent studies suggest the sound may be due to the filling ventricular wall hitting the inner chest wall, or it may arise from the ventricular apex as it hits a limitation of its longitudinal expansion.",True,unintrusive,,,,
264c35f4-cee6-44a2-95c5-7ea697baa3e5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,Table 5.2: Common causes of abnormal S3.,True,unintrusive,,,,
e92a45d8-1eab-4070-9e48-4a9035af48e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"As S3 is a filling sound, an abnormal S3 (higher pitch and referred to as a ventricular gallop) is an important clue to heart failure or volume overload (see table 5.2). The absence of an abnormal S3 does not rule out heart failure, but its presence is a sensitive indicator of ventricular dysfunction. Constriction around the heart (e.g., constrictive pericarditis) may cause an early S3, or “pericardial knock.”",True,unintrusive,,,,
86b88799-7eef-44ee-aec7-32e04289ed10,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"S4 is abnormal and is associated with poor ventricular compliance (e.g., ventricular hypertrophy). It occurs during atrial contraction and is associated with the atrial pressure pulse. The sound is thought to be caused by reverberation of the stiffened ventricular wall as blood is propelled into the ventricle from the atrium (hence it is also known as an atrial gallop). S4 and raised end-diastolic ventricular pressure (EDVP) commonly occur together as both are caused by poor ventricular compliance, so S4 tends to be associated with conditions that cause pressure overload (see table 5.3).",True,unintrusive,,,,
c7f76a8d-8fc9-4f71-8c4b-5c8e57a72dd3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,Table 5.3: Common causes of abnormal S4.,True,unintrusive,,,,
7d756952-018b-4b3c-9568-bf99a26aacd4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,Ejection Sounds (Clicks),False,Ejection Sounds (Clicks),,,,
33ff7da0-dd58-49b3-a035-3e485cd7b0a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"As S1 and S2 occur during closure of heart valves, pathological conditions can lead to the valves producing a high-frequency “clicking” sound when they open during chamber ejection—hence they can be referred to as ejection sounds and they are pathological.",True,Ejection Sounds (Clicks),,,,
682d057b-fb5b-49ad-8de3-b8f474d75478,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"Aortic ejection sounds usually occur 0.12–0.14 seconds after the Q-wave of the ECG (i.e., after ventricular pressure has risen to exceed aortic pressure). Because of its timing, the “click” produced can be misinterpreted as a split S1. The abnormal opening of the aortic valve is usually caused by a deformed but mobile valve leaflet or aortic root dilation that may be caused by the conditions listed in table 5.4.",True,Ejection Sounds (Clicks),,,,
b72dbfb3-e4d3-44ff-baed-da454fbae8ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"Pulmonary ejection sounds occur a little earlier (0.09–0.11 seconds) after the Q-wave as the pulmonary valve opens a little earlier (figure 5.1). It can also be distinguished by the fact that its intensity is diminished during inspiration as increased venous return during inspiration augments the effect of atrial contraction and causes a “gentler” opening of the valve. As with the aortic ejection sounds, pulmonary ejection sounds are associated with deformed valves or pulmonary arterial dilation.",True,Ejection Sounds (Clicks),Figure 5.1,Heart Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
b72dbfb3-e4d3-44ff-baed-da454fbae8ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"Pulmonary ejection sounds occur a little earlier (0.09–0.11 seconds) after the Q-wave as the pulmonary valve opens a little earlier (figure 5.1). It can also be distinguished by the fact that its intensity is diminished during inspiration as increased venous return during inspiration augments the effect of atrial contraction and causes a “gentler” opening of the valve. As with the aortic ejection sounds, pulmonary ejection sounds are associated with deformed valves or pulmonary arterial dilation.",True,Ejection Sounds (Clicks),Figure 5.1,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
b72dbfb3-e4d3-44ff-baed-da454fbae8ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"Pulmonary ejection sounds occur a little earlier (0.09–0.11 seconds) after the Q-wave as the pulmonary valve opens a little earlier (figure 5.1). It can also be distinguished by the fact that its intensity is diminished during inspiration as increased venous return during inspiration augments the effect of atrial contraction and causes a “gentler” opening of the valve. As with the aortic ejection sounds, pulmonary ejection sounds are associated with deformed valves or pulmonary arterial dilation.",True,Ejection Sounds (Clicks),Figure 5.1,Heart Sounds,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
b72dbfb3-e4d3-44ff-baed-da454fbae8ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"Pulmonary ejection sounds occur a little earlier (0.09–0.11 seconds) after the Q-wave as the pulmonary valve opens a little earlier (figure 5.1). It can also be distinguished by the fact that its intensity is diminished during inspiration as increased venous return during inspiration augments the effect of atrial contraction and causes a “gentler” opening of the valve. As with the aortic ejection sounds, pulmonary ejection sounds are associated with deformed valves or pulmonary arterial dilation.",True,Ejection Sounds (Clicks),Figure 5.1,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
dce0ee7c-bd1d-4e70-8180-f80a208666cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"A click occurring in diastole is associated with abnormal opening of either the mitral or tricuspid valve. Similar to systolic clicks, a diastolic click can be misinterpreted as a split S2. The most common cause of diastolic clicks is valvular stenosis of an AV valve.",True,Ejection Sounds (Clicks),,,,
b93f6e0a-c28d-4b6d-bfd2-6801e5600716,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"Table 5.4: Common causes of ejection ""clicks.""",True,Ejection Sounds (Clicks),,,,
63c79673-fd9f-4536-b671-5b80a88138d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,Heart Murmurs,False,Heart Murmurs,,,,
3f3a9904-25e0-43dd-a16d-6e01c6b13bfa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"A murmur is the sound of turbulence associated with abnormal blood flow through a valve or chamber. The turbulent flow produces low-frequency audible sounds that are distinct from heart sounds associated with valve closures. Murmurs can be divided into those caused by valvular defects and those caused by abnormal interchamber flow. Depending on the defect involved, the murmur may occur during diastole and systole, hence distinguishing whether a murmur is diastolic or systolic is a useful first diagnostic step.",True,Heart Murmurs,,,,
5349b6b4-dda7-40aa-94d4-cf1c75764156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"Classification of a murmur includes the intensity (Grades 1–6, faintest to loudest), the pitch (high or low), configuration, location, and timing. The timing refers to the onset and duration of the murmur, and the classifications are shown in table 5.5 with some common causes listed there and below.",True,Heart Murmurs,,,,
9204091b-4fe1-4364-9ec1-81e2ca72b30e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,Table 5.5: Classifications of heart murmurs.,True,Heart Murmurs,,,,
d5d1ace2-f402-485e-960b-c9543e1e62b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,Text,False,Text,,,,
89709126-33f3-4f93-8829-edc6986e3bcb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"Dornbush, Sean, and Andre E. Turnquest. Physiology, Heart Sounds. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK541010, CC BY 4.0.",True,Text,,,,
26c68188-310c-49ec-8107-6f74eb8e4e3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"Kulkarni, Vivek T., and Leonard S. Lilly. “The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 2. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
85fdbdb6-2d1c-453a-b06c-0104eabcc7b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"Thomas, Seth L., Joseph Heaton, and Amgad N. Makaryus. Physiology, Cardiovascular Murmurs. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK525958, CC BY 4.0.",True,Text,,,,
6df0f601-ce19-473b-bda3-69c7b3d93758,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Sounds,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/#chapter-38-section-1,"Table 5.5: Classifications of heart murmurs. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/5.5_20220113",True,Text,,,,
d025b1ce-e7f8-4920-8d3a-02dfe3b99e8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,unintrusive,False,unintrusive,,,,
819bf58b-fa3c-408f-aed1-d35637a32c26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,The first and second sounds (S1 and S2) are the fundamental heart sounds.,True,unintrusive,,,,
bbe59e79-24bd-4750-ac10-13b9dc42b4f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"S1 occurs at the beginning of isovolumetric contraction. The ventricle is beginning to contract, so ventricular pressure quickly rises above atrial pressure and the atrioventricular (tricuspid and mitral) valves close, producing the S1 sound. The mitral valve normally closes slightly (0.04 seconds) before the tricuspid, causing S1 to be “split” (i.e., actually being two sounds, M1 and T1 (figure 5.1)), but the time gap is too short with a normal heart to be detectable with a stethoscope. The reasons for M1 preceding T1 are not clear, but may be due to the force generation of the left ventricle being slightly faster than that of the right ventricle. The splitting of S1 can be more pronounced and audible in the presence of a right bundle branch block (figure 5.1) that causes left ventricular contraction (and mitral valve closure) to markedly precede contraction of the right ventricle. Conversely, in the case of a left bundle branch block, the normal splitting of S1 may be absent (figure 5.1) as M1 is delayed and so occurs in synchrony with T1.",True,unintrusive,Figure 5.1,Heart Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
bbe59e79-24bd-4750-ac10-13b9dc42b4f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"S1 occurs at the beginning of isovolumetric contraction. The ventricle is beginning to contract, so ventricular pressure quickly rises above atrial pressure and the atrioventricular (tricuspid and mitral) valves close, producing the S1 sound. The mitral valve normally closes slightly (0.04 seconds) before the tricuspid, causing S1 to be “split” (i.e., actually being two sounds, M1 and T1 (figure 5.1)), but the time gap is too short with a normal heart to be detectable with a stethoscope. The reasons for M1 preceding T1 are not clear, but may be due to the force generation of the left ventricle being slightly faster than that of the right ventricle. The splitting of S1 can be more pronounced and audible in the presence of a right bundle branch block (figure 5.1) that causes left ventricular contraction (and mitral valve closure) to markedly precede contraction of the right ventricle. Conversely, in the case of a left bundle branch block, the normal splitting of S1 may be absent (figure 5.1) as M1 is delayed and so occurs in synchrony with T1.",True,unintrusive,Figure 5.1,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
bbe59e79-24bd-4750-ac10-13b9dc42b4f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"S1 occurs at the beginning of isovolumetric contraction. The ventricle is beginning to contract, so ventricular pressure quickly rises above atrial pressure and the atrioventricular (tricuspid and mitral) valves close, producing the S1 sound. The mitral valve normally closes slightly (0.04 seconds) before the tricuspid, causing S1 to be “split” (i.e., actually being two sounds, M1 and T1 (figure 5.1)), but the time gap is too short with a normal heart to be detectable with a stethoscope. The reasons for M1 preceding T1 are not clear, but may be due to the force generation of the left ventricle being slightly faster than that of the right ventricle. The splitting of S1 can be more pronounced and audible in the presence of a right bundle branch block (figure 5.1) that causes left ventricular contraction (and mitral valve closure) to markedly precede contraction of the right ventricle. Conversely, in the case of a left bundle branch block, the normal splitting of S1 may be absent (figure 5.1) as M1 is delayed and so occurs in synchrony with T1.",True,unintrusive,Figure 5.1,Heart Sounds,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
bbe59e79-24bd-4750-ac10-13b9dc42b4f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"S1 occurs at the beginning of isovolumetric contraction. The ventricle is beginning to contract, so ventricular pressure quickly rises above atrial pressure and the atrioventricular (tricuspid and mitral) valves close, producing the S1 sound. The mitral valve normally closes slightly (0.04 seconds) before the tricuspid, causing S1 to be “split” (i.e., actually being two sounds, M1 and T1 (figure 5.1)), but the time gap is too short with a normal heart to be detectable with a stethoscope. The reasons for M1 preceding T1 are not clear, but may be due to the force generation of the left ventricle being slightly faster than that of the right ventricle. The splitting of S1 can be more pronounced and audible in the presence of a right bundle branch block (figure 5.1) that causes left ventricular contraction (and mitral valve closure) to markedly precede contraction of the right ventricle. Conversely, in the case of a left bundle branch block, the normal splitting of S1 may be absent (figure 5.1) as M1 is delayed and so occurs in synchrony with T1.",True,unintrusive,Figure 5.1,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
5c1f7356-69c3-44c2-a558-ff9c0840b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"S2 is caused by closure of the aortic and pulmonic valves at the beginning of isovolumetric ventricular relaxation when ventricular pressure falls below pulmonary and aortic pressure. As aortic pressure (80 mmHg) is far greater than pulmonary artery pressure (10 mmHg), S2 is normally split with two components (A2 and P2) relating to the closure of the aortic and pulmonic valves, respectively. How split A2 and P2 are depend on physiological conditions, primarily the phase of breathing that influences the pulmonary artery pressure. In expiration pulmonary artery pressure is higher, so the pulmonic valve closes earlier and P2 occurs closer to A2. Conversely, during inspiration pulmonary artery pressure falls, so pulmonic valve closing occurs later and A2 and P2 occur further apart (figure 5.2). This physiological splitting can be heard with a stethoscope, but can be further influenced by diseases as listed in table 5.1.",True,unintrusive,Figure 5.2,Heart Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.2-scaled.jpg,Figure 5.2: Normal splitting of S2 with inspiration.
5c1f7356-69c3-44c2-a558-ff9c0840b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"S2 is caused by closure of the aortic and pulmonic valves at the beginning of isovolumetric ventricular relaxation when ventricular pressure falls below pulmonary and aortic pressure. As aortic pressure (80 mmHg) is far greater than pulmonary artery pressure (10 mmHg), S2 is normally split with two components (A2 and P2) relating to the closure of the aortic and pulmonic valves, respectively. How split A2 and P2 are depend on physiological conditions, primarily the phase of breathing that influences the pulmonary artery pressure. In expiration pulmonary artery pressure is higher, so the pulmonic valve closes earlier and P2 occurs closer to A2. Conversely, during inspiration pulmonary artery pressure falls, so pulmonic valve closing occurs later and A2 and P2 occur further apart (figure 5.2). This physiological splitting can be heard with a stethoscope, but can be further influenced by diseases as listed in table 5.1.",True,unintrusive,Figure 5.2,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.2-scaled.jpg,Figure 5.2: Normal splitting of S2 with inspiration.
5c1f7356-69c3-44c2-a558-ff9c0840b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"S2 is caused by closure of the aortic and pulmonic valves at the beginning of isovolumetric ventricular relaxation when ventricular pressure falls below pulmonary and aortic pressure. As aortic pressure (80 mmHg) is far greater than pulmonary artery pressure (10 mmHg), S2 is normally split with two components (A2 and P2) relating to the closure of the aortic and pulmonic valves, respectively. How split A2 and P2 are depend on physiological conditions, primarily the phase of breathing that influences the pulmonary artery pressure. In expiration pulmonary artery pressure is higher, so the pulmonic valve closes earlier and P2 occurs closer to A2. Conversely, during inspiration pulmonary artery pressure falls, so pulmonic valve closing occurs later and A2 and P2 occur further apart (figure 5.2). This physiological splitting can be heard with a stethoscope, but can be further influenced by diseases as listed in table 5.1.",True,unintrusive,Figure 5.2,Heart Sounds,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.2-scaled.jpg,Figure 5.2: Normal splitting of S2 with inspiration.
5c1f7356-69c3-44c2-a558-ff9c0840b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"S2 is caused by closure of the aortic and pulmonic valves at the beginning of isovolumetric ventricular relaxation when ventricular pressure falls below pulmonary and aortic pressure. As aortic pressure (80 mmHg) is far greater than pulmonary artery pressure (10 mmHg), S2 is normally split with two components (A2 and P2) relating to the closure of the aortic and pulmonic valves, respectively. How split A2 and P2 are depend on physiological conditions, primarily the phase of breathing that influences the pulmonary artery pressure. In expiration pulmonary artery pressure is higher, so the pulmonic valve closes earlier and P2 occurs closer to A2. Conversely, during inspiration pulmonary artery pressure falls, so pulmonic valve closing occurs later and A2 and P2 occur further apart (figure 5.2). This physiological splitting can be heard with a stethoscope, but can be further influenced by diseases as listed in table 5.1.",True,unintrusive,Figure 5.2,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.2-scaled.jpg,Figure 5.2: Normal splitting of S2 with inspiration.
c4abf1d1-8f22-4447-b8fe-b8bde367992c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,Table 5.1: Changes in S2 splitting and possible underlying causes.,True,unintrusive,,,,
59d87209-7bdc-4aa4-a384-d703be139679,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"S3 is associated with the rapid filling phase of the ventricle (when the AV valves open), about 0.14 to 0.16 seconds after S2 (closure of the aortic and pulmonic valves). The exact cause of the sound is unclear, but a normal S3 occurs as a brief, low-frequency vibration. Previously thought to be an intracardiac sound arising from vibrations in the valve cusps or ventricular wall, more recent studies suggest the sound may be due to the filling ventricular wall hitting the inner chest wall, or it may arise from the ventricular apex as it hits a limitation of its longitudinal expansion.",True,unintrusive,,,,
81d3b752-543b-42b1-a51f-52fba0b568ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,Table 5.2: Common causes of abnormal S3.,True,unintrusive,,,,
0b4f791b-9407-47fa-81cb-e8ac19cdbb03,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"As S3 is a filling sound, an abnormal S3 (higher pitch and referred to as a ventricular gallop) is an important clue to heart failure or volume overload (see table 5.2). The absence of an abnormal S3 does not rule out heart failure, but its presence is a sensitive indicator of ventricular dysfunction. Constriction around the heart (e.g., constrictive pericarditis) may cause an early S3, or “pericardial knock.”",True,unintrusive,,,,
14d0c33f-1ed9-4f0d-8988-7a84222ed84b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"S4 is abnormal and is associated with poor ventricular compliance (e.g., ventricular hypertrophy). It occurs during atrial contraction and is associated with the atrial pressure pulse. The sound is thought to be caused by reverberation of the stiffened ventricular wall as blood is propelled into the ventricle from the atrium (hence it is also known as an atrial gallop). S4 and raised end-diastolic ventricular pressure (EDVP) commonly occur together as both are caused by poor ventricular compliance, so S4 tends to be associated with conditions that cause pressure overload (see table 5.3).",True,unintrusive,,,,
90b8c638-127a-46a0-88eb-365896204baa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,Table 5.3: Common causes of abnormal S4.,True,unintrusive,,,,
5151d662-8f7a-41a3-8503-989cb82f3015,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,Ejection Sounds (Clicks),False,Ejection Sounds (Clicks),,,,
4daecf91-6a9d-4707-8110-ae3387b52f52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"As S1 and S2 occur during closure of heart valves, pathological conditions can lead to the valves producing a high-frequency “clicking” sound when they open during chamber ejection—hence they can be referred to as ejection sounds and they are pathological.",True,Ejection Sounds (Clicks),,,,
c4d5ee35-aeca-4c05-a357-4102c408b0f3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"Aortic ejection sounds usually occur 0.12–0.14 seconds after the Q-wave of the ECG (i.e., after ventricular pressure has risen to exceed aortic pressure). Because of its timing, the “click” produced can be misinterpreted as a split S1. The abnormal opening of the aortic valve is usually caused by a deformed but mobile valve leaflet or aortic root dilation that may be caused by the conditions listed in table 5.4.",True,Ejection Sounds (Clicks),,,,
99973ea6-9430-46e8-9b01-8629654f7dfd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"Pulmonary ejection sounds occur a little earlier (0.09–0.11 seconds) after the Q-wave as the pulmonary valve opens a little earlier (figure 5.1). It can also be distinguished by the fact that its intensity is diminished during inspiration as increased venous return during inspiration augments the effect of atrial contraction and causes a “gentler” opening of the valve. As with the aortic ejection sounds, pulmonary ejection sounds are associated with deformed valves or pulmonary arterial dilation.",True,Ejection Sounds (Clicks),Figure 5.1,Heart Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
99973ea6-9430-46e8-9b01-8629654f7dfd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"Pulmonary ejection sounds occur a little earlier (0.09–0.11 seconds) after the Q-wave as the pulmonary valve opens a little earlier (figure 5.1). It can also be distinguished by the fact that its intensity is diminished during inspiration as increased venous return during inspiration augments the effect of atrial contraction and causes a “gentler” opening of the valve. As with the aortic ejection sounds, pulmonary ejection sounds are associated with deformed valves or pulmonary arterial dilation.",True,Ejection Sounds (Clicks),Figure 5.1,Ejection Sounds (Clicks),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
99973ea6-9430-46e8-9b01-8629654f7dfd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"Pulmonary ejection sounds occur a little earlier (0.09–0.11 seconds) after the Q-wave as the pulmonary valve opens a little earlier (figure 5.1). It can also be distinguished by the fact that its intensity is diminished during inspiration as increased venous return during inspiration augments the effect of atrial contraction and causes a “gentler” opening of the valve. As with the aortic ejection sounds, pulmonary ejection sounds are associated with deformed valves or pulmonary arterial dilation.",True,Ejection Sounds (Clicks),Figure 5.1,Heart Sounds,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
99973ea6-9430-46e8-9b01-8629654f7dfd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"Pulmonary ejection sounds occur a little earlier (0.09–0.11 seconds) after the Q-wave as the pulmonary valve opens a little earlier (figure 5.1). It can also be distinguished by the fact that its intensity is diminished during inspiration as increased venous return during inspiration augments the effect of atrial contraction and causes a “gentler” opening of the valve. As with the aortic ejection sounds, pulmonary ejection sounds are associated with deformed valves or pulmonary arterial dilation.",True,Ejection Sounds (Clicks),Figure 5.1,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/5.1-scaled.jpg,Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).
f873a596-aafe-4515-9ba0-146e6ac61a8b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"A click occurring in diastole is associated with abnormal opening of either the mitral or tricuspid valve. Similar to systolic clicks, a diastolic click can be misinterpreted as a split S2. The most common cause of diastolic clicks is valvular stenosis of an AV valve.",True,Ejection Sounds (Clicks),,,,
5474920d-4fb6-4435-8b24-97132683b8ff,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"Table 5.4: Common causes of ejection ""clicks.""",True,Ejection Sounds (Clicks),,,,
2d0439d3-b99f-474b-9f6a-c77dac33cb6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,Heart Murmurs,False,Heart Murmurs,,,,
eebd529d-c331-4b7d-9341-0fa5588ed5b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"A murmur is the sound of turbulence associated with abnormal blood flow through a valve or chamber. The turbulent flow produces low-frequency audible sounds that are distinct from heart sounds associated with valve closures. Murmurs can be divided into those caused by valvular defects and those caused by abnormal interchamber flow. Depending on the defect involved, the murmur may occur during diastole and systole, hence distinguishing whether a murmur is diastolic or systolic is a useful first diagnostic step.",True,Heart Murmurs,,,,
1b765788-a792-48bf-a32d-e67d3b337663,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"Classification of a murmur includes the intensity (Grades 1–6, faintest to loudest), the pitch (high or low), configuration, location, and timing. The timing refers to the onset and duration of the murmur, and the classifications are shown in table 5.5 with some common causes listed there and below.",True,Heart Murmurs,,,,
23ad8795-df21-44df-9b08-546ac090dc7e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,Table 5.5: Classifications of heart murmurs.,True,Heart Murmurs,,,,
eb85441d-feb7-45ea-a295-854b15a88493,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,Text,False,Text,,,,
34a45943-4200-447d-9536-52d792bd15c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"Dornbush, Sean, and Andre E. Turnquest. Physiology, Heart Sounds. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK541010, CC BY 4.0.",True,Text,,,,
f4e029d2-aba0-4dcc-8a1a-f1cf4acf1f19,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"Kulkarni, Vivek T., and Leonard S. Lilly. “The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 2. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
4b77cc1e-c647-46f8-b8fc-867d79494802,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"Thomas, Seth L., Joseph Heaton, and Amgad N. Makaryus. Physiology, Cardiovascular Murmurs. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK525958, CC BY 4.0.",True,Text,,,,
37a7a155-b41b-435a-a5d9-5480449e5556,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,5. Heart Sounds and Murmurs,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-5-heart-sounds-and-murmurs/,"Table 5.5: Classifications of heart murmurs. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/5.5_20220113",True,Text,,,,
0d9a3874-61bf-4706-bc3b-cd7d9ea2021c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Abnormalities of valvular structure and/or function can either be congenital or acquired. Acquired valvular disease is by far the most common and is most prevalent in the elderly. The high blood flow and pressures that valves are exposed to make them particularly susceptible to other risk factors that promote valvular damage (see table 4.1). Congenital valvular defects arise from disrupted heart development, about 50 percent of which involve the valves. The impact of congenital defects has diminished with the advent of advanced detection techniques. What we will spend time on in this chapter is the main instigating factors and pathologies that result in acquired valvular defects.",True,Text,,,,
ccc9c78e-3005-40ab-baac-35ac9036e771,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,Table 4.1: Risk factors for acquired valvular damage.,True,Text,,,,
9098edeb-f4b5-4b10-aa41-7ecc7e039310,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
9098edeb-f4b5-4b10-aa41-7ecc7e039310,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
9098edeb-f4b5-4b10-aa41-7ecc7e039310,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
9098edeb-f4b5-4b10-aa41-7ecc7e039310,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
9098edeb-f4b5-4b10-aa41-7ecc7e039310,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
9098edeb-f4b5-4b10-aa41-7ecc7e039310,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
9098edeb-f4b5-4b10-aa41-7ecc7e039310,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
8e9c7284-ff78-4170-bdb5-1bb9aa034b4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"As they face the most pressure, the aortic and mitral valves are more prone to calcification. The most common pattern of calcification in the aortic valve is mounded masses within the cusps of the valve (see table 4.2) that eventually fuse and stop the valve from opening fully. Calcification in the mitral valve tends to start in the fibrous annulus, which does not impact valvular function to the same extent, but in exceptional cases can cause regurgitation or stenosis, or even arrhythmias as calcium deposits impinge on the atrioventricular conduction system (see table 4.2).",True,Text,,,,
56ee9369-4764-475a-bf47-8192d06fa092,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,Table 4.2: Location of calcium deposits on aortic and mitral valves and their pathological consequences.,True,Text,,,,
d0b0605b-9171-49cc-a037-2b1824b6be14,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,Mitral Valve Prolapse (MVP),False,Mitral Valve Prolapse (MVP),,,,
25e1bb25-ef77-49ee-becc-697b567b01d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
25e1bb25-ef77-49ee-becc-697b567b01d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
25e1bb25-ef77-49ee-becc-697b567b01d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
25e1bb25-ef77-49ee-becc-697b567b01d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
25e1bb25-ef77-49ee-becc-697b567b01d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
25e1bb25-ef77-49ee-becc-697b567b01d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
25e1bb25-ef77-49ee-becc-697b567b01d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
83ad3463-bd48-4a5d-9550-96ee5e4586ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The causes of MVP are usually unidentified, but a few cases can be attributed to inherited connective tissue disorders such as Marfan syndrome. The prolapsed valve leaflet composition is enlarged and thickened with deposition of myxomatous material rich in proteoglycans, and a reduction in the structurally critical fibrosa layer where a higher prevalence of type III collagen (a more stretchy than structural form of collagen) is found.",True,Mitral Valve Prolapse (MVP),,,,
3830bcdf-10ca-46bc-b1c6-da084e9eb154,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The flapping valve structure can cause secondary fibrosis on the structures it strikes, such as the leaflet edges or the endocardium where the abnormally elongated cords rub. The agitation may also promote thrombus formation in the atrium.",True,Mitral Valve Prolapse (MVP),,,,
071facc2-9ef2-4958-bb2d-ef391a7e20cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
071facc2-9ef2-4958-bb2d-ef391a7e20cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
071facc2-9ef2-4958-bb2d-ef391a7e20cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
071facc2-9ef2-4958-bb2d-ef391a7e20cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
071facc2-9ef2-4958-bb2d-ef391a7e20cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
071facc2-9ef2-4958-bb2d-ef391a7e20cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
071facc2-9ef2-4958-bb2d-ef391a7e20cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
7bb51be0-96d8-496d-8012-70b75e35f133,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,Rheumatic Heart Disease,False,Rheumatic Heart Disease,,,,
2093f797-eecd-4860-b20e-322f80a0b697,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Rheumatic heart disease (RHD) is virtually the only cause of mitral valve stenosis. It arises after a group A streptococcal infection that often originates in the upper airway and leads to rheumatic fever (a multisystem, immune-mediated disease). The incidence in developed countries is relatively low because of rapid diagnosis and treatment of the instigating pharyngitis, but in poor, crowed, urban areas RHD remains an important health issue.",True,Rheumatic Heart Disease,,,,
360fb267-07a9-402e-9a7e-438c6986ea70,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The acute results of rheumatic fever occur days to weeks after the streptococcal infection, and while the initial pharyngeal infection may have cleared and the test results have become negative, the antibodies to the streptococcal enzymes (Streptolysin O and DNase B) can still be detected. The initial cardiac effects include carditis, pericardial rubs, tachycardia, and arrhythmias. However, the chronic effects may arise years or even decades later.",True,Rheumatic Heart Disease,,,,
e933abed-192e-441f-b157-fbf11ce31326,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
e933abed-192e-441f-b157-fbf11ce31326,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
e933abed-192e-441f-b157-fbf11ce31326,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
e933abed-192e-441f-b157-fbf11ce31326,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
e933abed-192e-441f-b157-fbf11ce31326,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
e933abed-192e-441f-b157-fbf11ce31326,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
e933abed-192e-441f-b157-fbf11ce31326,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
fabf8aa6-13d8-4527-8773-5aaca4242bc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
fabf8aa6-13d8-4527-8773-5aaca4242bc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
fabf8aa6-13d8-4527-8773-5aaca4242bc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
fabf8aa6-13d8-4527-8773-5aaca4242bc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
fabf8aa6-13d8-4527-8773-5aaca4242bc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
fabf8aa6-13d8-4527-8773-5aaca4242bc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
fabf8aa6-13d8-4527-8773-5aaca4242bc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
0ebbe1a6-cda0-4ef4-aaf0-d105344147e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,Infective Endocarditis,False,Infective Endocarditis,,,,
4d708ee1-4455-43f5-bbcf-2b98b7d02e96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Infective endocarditis (IE) is divided into acute and subacute forms, depending on the virulence of the causal pathogen. Acute IE is rapid in onset and involves highly destructive pathogens that cause necrosis and significant lesions that can lead to death in a matter of days. Subacute IE, alternatively, can deform the valves over weeks to months and generally involves a much less destructive pathogen.",True,Infective Endocarditis,,,,
b4efabae-c886-41e7-afdd-30e3c3e1fde1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Acute cases tend to involve healthy individuals and are responsible for 20 to 30 percent of cases, whereas the less virulent pathogens that cause subacute IE tend to need a foothold and only affect previously damaged or deformed valves.",True,Infective Endocarditis,,,,
208863b0-d700-491e-a56c-57d15fcf0459,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
208863b0-d700-491e-a56c-57d15fcf0459,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
208863b0-d700-491e-a56c-57d15fcf0459,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
208863b0-d700-491e-a56c-57d15fcf0459,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
208863b0-d700-491e-a56c-57d15fcf0459,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
208863b0-d700-491e-a56c-57d15fcf0459,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
208863b0-d700-491e-a56c-57d15fcf0459,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
04cf7a1f-a0b1-4e9c-bb8a-d473cd9f1098,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,The risk is twofold as the vegetations can:,False,The risk is twofold as the vegetations can:,,,,
2ada3b7c-1dd9-4458-a070-a1cf8b01ba05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
2ada3b7c-1dd9-4458-a070-a1cf8b01ba05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
2ada3b7c-1dd9-4458-a070-a1cf8b01ba05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
2ada3b7c-1dd9-4458-a070-a1cf8b01ba05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
2ada3b7c-1dd9-4458-a070-a1cf8b01ba05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
2ada3b7c-1dd9-4458-a070-a1cf8b01ba05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
2ada3b7c-1dd9-4458-a070-a1cf8b01ba05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
99aa4115-b5d2-4ffa-967a-744f26be09fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,Noninfective Vegetations,False,Noninfective Vegetations,,,,
d7a40cbf-0c72-4cc8-9b48-8f359276ee39,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Some vegetations are sterile (i.e., occur in the absence of infection). There are two main examples of this—nonbacterial thrombotic endocarditis (NBTE) and the systemic lupus erythematosus (SLE).",True,Noninfective Vegetations,,,,
9735b804-9384-4972-8801-65b4137d8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
9735b804-9384-4972-8801-65b4137d8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
9735b804-9384-4972-8801-65b4137d8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
9735b804-9384-4972-8801-65b4137d8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
9735b804-9384-4972-8801-65b4137d8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
9735b804-9384-4972-8801-65b4137d8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
9735b804-9384-4972-8801-65b4137d8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
fc5b8240-74d4-4363-8ff2-89da75b67d46,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
fc5b8240-74d4-4363-8ff2-89da75b67d46,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
fc5b8240-74d4-4363-8ff2-89da75b67d46,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
fc5b8240-74d4-4363-8ff2-89da75b67d46,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
fc5b8240-74d4-4363-8ff2-89da75b67d46,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
fc5b8240-74d4-4363-8ff2-89da75b67d46,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
fc5b8240-74d4-4363-8ff2-89da75b67d46,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
1a5ae73c-60e1-4608-842e-4bd4e79ff4cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,Carcinoid Heart Disease,False,Carcinoid Heart Disease,,,,
4951a27c-fe47-412b-a160-ced605a85c96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
4951a27c-fe47-412b-a160-ced605a85c96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
4951a27c-fe47-412b-a160-ced605a85c96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
4951a27c-fe47-412b-a160-ced605a85c96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
4951a27c-fe47-412b-a160-ced605a85c96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
4951a27c-fe47-412b-a160-ced605a85c96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
4951a27c-fe47-412b-a160-ced605a85c96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
f5fc14dc-e762-4dc2-9c28-aefe679a91e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"The liver normally metabolizes these circulating mediators, but when the metastatic burden overwhelms hepatic clearance, the right heart is exposed to their effects (the left heart is somewhat protected by the degradation performed by the pulmonary circulation).",True,Carcinoid Heart Disease,,,,
66efaec5-1124-469a-b63e-a04259cca668,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
66efaec5-1124-469a-b63e-a04259cca668,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
66efaec5-1124-469a-b63e-a04259cca668,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
66efaec5-1124-469a-b63e-a04259cca668,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
66efaec5-1124-469a-b63e-a04259cca668,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
66efaec5-1124-469a-b63e-a04259cca668,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
66efaec5-1124-469a-b63e-a04259cca668,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
9818c5d4-d694-4e91-b91d-1e1b840abe78,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,Text,False,Text,,,,
87a6622f-680a-4032-acf2-22d1a3d06a57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Dass, Clarissa, and Arun Kanmanthareddy. Rheumatic Heart Disease. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK538286/, CC BY 4.0.",True,Text,,,,
01571255-0baf-4ad1-abdb-c3c38901b4f1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Douedi, Steven, and Hani Douedi. Mitral Regurgitation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK553135/, CC BY 4.0.",True,Text,,,,
7f9e8792-d353-4380-b72b-10095d2e32d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Lopez, Diana M., Patrick T. O’Gara, and Leonard S. Lilly. “Valvular Heart  Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 8. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
0b92e173-7511-4e4f-a01c-46a261d63327,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Wenn, Peter, and Roman Zeltser. Aortic Valve Disease. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK542205/, CC BY 4.0.",True,Text,,,,
1ae0ec16-694d-4b2e-9c46-4f16ca1187bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-6,"Table 4.1: Location of calcium deposits on aortic and mitral valves and their pathological consequences. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/4.2a_20220113",True,Text,,,,
ac85bf9e-157e-4cb1-b55b-f1efe2e59a59,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Abnormalities of valvular structure and/or function can either be congenital or acquired. Acquired valvular disease is by far the most common and is most prevalent in the elderly. The high blood flow and pressures that valves are exposed to make them particularly susceptible to other risk factors that promote valvular damage (see table 4.1). Congenital valvular defects arise from disrupted heart development, about 50 percent of which involve the valves. The impact of congenital defects has diminished with the advent of advanced detection techniques. What we will spend time on in this chapter is the main instigating factors and pathologies that result in acquired valvular defects.",True,Text,,,,
5fd7f6f2-575a-479f-90d6-1ceb32540da6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,Table 4.1: Risk factors for acquired valvular damage.,True,Text,,,,
fa42fa94-e72b-4338-90b4-83dacc3f6505,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
fa42fa94-e72b-4338-90b4-83dacc3f6505,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
fa42fa94-e72b-4338-90b4-83dacc3f6505,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
fa42fa94-e72b-4338-90b4-83dacc3f6505,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
fa42fa94-e72b-4338-90b4-83dacc3f6505,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
fa42fa94-e72b-4338-90b4-83dacc3f6505,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
fa42fa94-e72b-4338-90b4-83dacc3f6505,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
012df42d-646f-40f7-a68f-b628cb1c1678,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"As they face the most pressure, the aortic and mitral valves are more prone to calcification. The most common pattern of calcification in the aortic valve is mounded masses within the cusps of the valve (see table 4.2) that eventually fuse and stop the valve from opening fully. Calcification in the mitral valve tends to start in the fibrous annulus, which does not impact valvular function to the same extent, but in exceptional cases can cause regurgitation or stenosis, or even arrhythmias as calcium deposits impinge on the atrioventricular conduction system (see table 4.2).",True,Text,,,,
2505ea6b-1d12-4aee-9157-c76f45cb6468,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,Table 4.2: Location of calcium deposits on aortic and mitral valves and their pathological consequences.,True,Text,,,,
83b8484f-c4e5-4ae3-92d7-e727d85f7f50,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,Mitral Valve Prolapse (MVP),False,Mitral Valve Prolapse (MVP),,,,
3a7f2627-b213-431e-ad48-2e49939678d8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
3a7f2627-b213-431e-ad48-2e49939678d8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
3a7f2627-b213-431e-ad48-2e49939678d8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
3a7f2627-b213-431e-ad48-2e49939678d8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
3a7f2627-b213-431e-ad48-2e49939678d8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
3a7f2627-b213-431e-ad48-2e49939678d8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
3a7f2627-b213-431e-ad48-2e49939678d8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
d4e1952b-f0bb-4f80-9414-c51926e6658c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The causes of MVP are usually unidentified, but a few cases can be attributed to inherited connective tissue disorders such as Marfan syndrome. The prolapsed valve leaflet composition is enlarged and thickened with deposition of myxomatous material rich in proteoglycans, and a reduction in the structurally critical fibrosa layer where a higher prevalence of type III collagen (a more stretchy than structural form of collagen) is found.",True,Mitral Valve Prolapse (MVP),,,,
be53d5e7-3e18-4fae-9330-6b723631febb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The flapping valve structure can cause secondary fibrosis on the structures it strikes, such as the leaflet edges or the endocardium where the abnormally elongated cords rub. The agitation may also promote thrombus formation in the atrium.",True,Mitral Valve Prolapse (MVP),,,,
63e772d5-e661-4e9d-bd87-c2277a12d009,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
63e772d5-e661-4e9d-bd87-c2277a12d009,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
63e772d5-e661-4e9d-bd87-c2277a12d009,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
63e772d5-e661-4e9d-bd87-c2277a12d009,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
63e772d5-e661-4e9d-bd87-c2277a12d009,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
63e772d5-e661-4e9d-bd87-c2277a12d009,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
63e772d5-e661-4e9d-bd87-c2277a12d009,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
74b820a8-9a15-46f3-946d-9f022bc3038e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,Rheumatic Heart Disease,False,Rheumatic Heart Disease,,,,
ec5c3783-debb-481c-ba4e-3d69bc427be6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Rheumatic heart disease (RHD) is virtually the only cause of mitral valve stenosis. It arises after a group A streptococcal infection that often originates in the upper airway and leads to rheumatic fever (a multisystem, immune-mediated disease). The incidence in developed countries is relatively low because of rapid diagnosis and treatment of the instigating pharyngitis, but in poor, crowed, urban areas RHD remains an important health issue.",True,Rheumatic Heart Disease,,,,
0067e0b1-3c01-48b4-bfac-9eaff9385bed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The acute results of rheumatic fever occur days to weeks after the streptococcal infection, and while the initial pharyngeal infection may have cleared and the test results have become negative, the antibodies to the streptococcal enzymes (Streptolysin O and DNase B) can still be detected. The initial cardiac effects include carditis, pericardial rubs, tachycardia, and arrhythmias. However, the chronic effects may arise years or even decades later.",True,Rheumatic Heart Disease,,,,
a9778d70-8a0d-45a7-b531-665b25842b2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
a9778d70-8a0d-45a7-b531-665b25842b2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
a9778d70-8a0d-45a7-b531-665b25842b2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
a9778d70-8a0d-45a7-b531-665b25842b2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
a9778d70-8a0d-45a7-b531-665b25842b2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
a9778d70-8a0d-45a7-b531-665b25842b2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
a9778d70-8a0d-45a7-b531-665b25842b2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
eb5c58f2-81d8-450f-91aa-79c9a12b278d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
eb5c58f2-81d8-450f-91aa-79c9a12b278d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
eb5c58f2-81d8-450f-91aa-79c9a12b278d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
eb5c58f2-81d8-450f-91aa-79c9a12b278d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
eb5c58f2-81d8-450f-91aa-79c9a12b278d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
eb5c58f2-81d8-450f-91aa-79c9a12b278d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
eb5c58f2-81d8-450f-91aa-79c9a12b278d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
f451a4b0-aa96-4d08-abd2-6984befb1292,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,Infective Endocarditis,False,Infective Endocarditis,,,,
02797ac0-9fad-45e7-9edf-6dfbc695bdd6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Infective endocarditis (IE) is divided into acute and subacute forms, depending on the virulence of the causal pathogen. Acute IE is rapid in onset and involves highly destructive pathogens that cause necrosis and significant lesions that can lead to death in a matter of days. Subacute IE, alternatively, can deform the valves over weeks to months and generally involves a much less destructive pathogen.",True,Infective Endocarditis,,,,
3043c1d3-6f4c-4da9-aced-eef67668e956,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Acute cases tend to involve healthy individuals and are responsible for 20 to 30 percent of cases, whereas the less virulent pathogens that cause subacute IE tend to need a foothold and only affect previously damaged or deformed valves.",True,Infective Endocarditis,,,,
dec01a89-e817-46ab-b069-ce90d555e9c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
dec01a89-e817-46ab-b069-ce90d555e9c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
dec01a89-e817-46ab-b069-ce90d555e9c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
dec01a89-e817-46ab-b069-ce90d555e9c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
dec01a89-e817-46ab-b069-ce90d555e9c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
dec01a89-e817-46ab-b069-ce90d555e9c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
dec01a89-e817-46ab-b069-ce90d555e9c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
d6d97053-b65e-4731-a9f4-ff38a6864fea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,The risk is twofold as the vegetations can:,False,The risk is twofold as the vegetations can:,,,,
4c5e4e1a-9dfe-4db6-b24f-d897db16b755,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
4c5e4e1a-9dfe-4db6-b24f-d897db16b755,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
4c5e4e1a-9dfe-4db6-b24f-d897db16b755,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
4c5e4e1a-9dfe-4db6-b24f-d897db16b755,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
4c5e4e1a-9dfe-4db6-b24f-d897db16b755,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
4c5e4e1a-9dfe-4db6-b24f-d897db16b755,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
4c5e4e1a-9dfe-4db6-b24f-d897db16b755,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
eae43628-63aa-49c1-b86d-378500b90a2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,Noninfective Vegetations,False,Noninfective Vegetations,,,,
f421c1ea-c6ef-4d66-ad5e-f3bf3aac2ec2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Some vegetations are sterile (i.e., occur in the absence of infection). There are two main examples of this—nonbacterial thrombotic endocarditis (NBTE) and the systemic lupus erythematosus (SLE).",True,Noninfective Vegetations,,,,
ab002e34-53ea-49a2-bb79-7eebe1166ece,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
ab002e34-53ea-49a2-bb79-7eebe1166ece,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
ab002e34-53ea-49a2-bb79-7eebe1166ece,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
ab002e34-53ea-49a2-bb79-7eebe1166ece,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
ab002e34-53ea-49a2-bb79-7eebe1166ece,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
ab002e34-53ea-49a2-bb79-7eebe1166ece,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
ab002e34-53ea-49a2-bb79-7eebe1166ece,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
532cf110-c8bf-49d7-b30c-5f6e28d3e701,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
532cf110-c8bf-49d7-b30c-5f6e28d3e701,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
532cf110-c8bf-49d7-b30c-5f6e28d3e701,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
532cf110-c8bf-49d7-b30c-5f6e28d3e701,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
532cf110-c8bf-49d7-b30c-5f6e28d3e701,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
532cf110-c8bf-49d7-b30c-5f6e28d3e701,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
532cf110-c8bf-49d7-b30c-5f6e28d3e701,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
3c0c4c2f-ff35-48af-a501-a9f2ab6e49b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,Carcinoid Heart Disease,False,Carcinoid Heart Disease,,,,
dd73608b-90c9-403e-847e-3cd956d87d9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
dd73608b-90c9-403e-847e-3cd956d87d9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
dd73608b-90c9-403e-847e-3cd956d87d9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
dd73608b-90c9-403e-847e-3cd956d87d9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
dd73608b-90c9-403e-847e-3cd956d87d9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
dd73608b-90c9-403e-847e-3cd956d87d9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
dd73608b-90c9-403e-847e-3cd956d87d9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
093a5c4e-46e2-49bf-a40c-d2c12e03158e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"The liver normally metabolizes these circulating mediators, but when the metastatic burden overwhelms hepatic clearance, the right heart is exposed to their effects (the left heart is somewhat protected by the degradation performed by the pulmonary circulation).",True,Carcinoid Heart Disease,,,,
e9de209c-3f32-45a9-9bd6-00d27a687367,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
e9de209c-3f32-45a9-9bd6-00d27a687367,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
e9de209c-3f32-45a9-9bd6-00d27a687367,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
e9de209c-3f32-45a9-9bd6-00d27a687367,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
e9de209c-3f32-45a9-9bd6-00d27a687367,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
e9de209c-3f32-45a9-9bd6-00d27a687367,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
e9de209c-3f32-45a9-9bd6-00d27a687367,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
2618fa34-8a21-4155-90c7-1e673b8cfcad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,Text,False,Text,,,,
92a19548-3b7a-46a3-9ad4-524a2bbc54bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Dass, Clarissa, and Arun Kanmanthareddy. Rheumatic Heart Disease. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK538286/, CC BY 4.0.",True,Text,,,,
846f187a-cb87-411e-aa41-bde8ff791dfd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Douedi, Steven, and Hani Douedi. Mitral Regurgitation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK553135/, CC BY 4.0.",True,Text,,,,
004a6235-610d-4796-8986-ff7e6e4b3aa5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Lopez, Diana M., Patrick T. O’Gara, and Leonard S. Lilly. “Valvular Heart  Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 8. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
fc63cfa0-0044-4b7e-b598-b88b8229fb3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Wenn, Peter, and Roman Zeltser. Aortic Valve Disease. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK542205/, CC BY 4.0.",True,Text,,,,
36929319-eb31-4f95-ab47-cc8f5a22b517,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Noninfective Vegetations,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-5,"Table 4.1: Location of calcium deposits on aortic and mitral valves and their pathological consequences. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/4.2a_20220113",True,Text,,,,
bc206dc1-0c69-4d63-ba75-ee9851873a1b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Abnormalities of valvular structure and/or function can either be congenital or acquired. Acquired valvular disease is by far the most common and is most prevalent in the elderly. The high blood flow and pressures that valves are exposed to make them particularly susceptible to other risk factors that promote valvular damage (see table 4.1). Congenital valvular defects arise from disrupted heart development, about 50 percent of which involve the valves. The impact of congenital defects has diminished with the advent of advanced detection techniques. What we will spend time on in this chapter is the main instigating factors and pathologies that result in acquired valvular defects.",True,Text,,,,
a8a81579-5b56-452f-9e70-315e897e7112,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,Table 4.1: Risk factors for acquired valvular damage.,True,Text,,,,
d69c0f3f-5a71-44e2-86e3-c13988424fde,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
d69c0f3f-5a71-44e2-86e3-c13988424fde,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
d69c0f3f-5a71-44e2-86e3-c13988424fde,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
d69c0f3f-5a71-44e2-86e3-c13988424fde,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
d69c0f3f-5a71-44e2-86e3-c13988424fde,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
d69c0f3f-5a71-44e2-86e3-c13988424fde,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
d69c0f3f-5a71-44e2-86e3-c13988424fde,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
d4c2a20f-2791-4a56-b9ba-0d77f59561fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"As they face the most pressure, the aortic and mitral valves are more prone to calcification. The most common pattern of calcification in the aortic valve is mounded masses within the cusps of the valve (see table 4.2) that eventually fuse and stop the valve from opening fully. Calcification in the mitral valve tends to start in the fibrous annulus, which does not impact valvular function to the same extent, but in exceptional cases can cause regurgitation or stenosis, or even arrhythmias as calcium deposits impinge on the atrioventricular conduction system (see table 4.2).",True,Text,,,,
efc66e96-3483-47f4-aa4c-79050ecbec61,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,Table 4.2: Location of calcium deposits on aortic and mitral valves and their pathological consequences.,True,Text,,,,
2341a4cf-29fb-4fcf-993e-5940b333139d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,Mitral Valve Prolapse (MVP),False,Mitral Valve Prolapse (MVP),,,,
3b7d59e1-0b76-45cb-88bf-459414a5a860,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
3b7d59e1-0b76-45cb-88bf-459414a5a860,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
3b7d59e1-0b76-45cb-88bf-459414a5a860,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
3b7d59e1-0b76-45cb-88bf-459414a5a860,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
3b7d59e1-0b76-45cb-88bf-459414a5a860,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
3b7d59e1-0b76-45cb-88bf-459414a5a860,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
3b7d59e1-0b76-45cb-88bf-459414a5a860,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
953c4f99-489d-45b2-a926-fac33029b919,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The causes of MVP are usually unidentified, but a few cases can be attributed to inherited connective tissue disorders such as Marfan syndrome. The prolapsed valve leaflet composition is enlarged and thickened with deposition of myxomatous material rich in proteoglycans, and a reduction in the structurally critical fibrosa layer where a higher prevalence of type III collagen (a more stretchy than structural form of collagen) is found.",True,Mitral Valve Prolapse (MVP),,,,
b65b8210-67fc-4a45-bb9d-db6631ac9e51,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The flapping valve structure can cause secondary fibrosis on the structures it strikes, such as the leaflet edges or the endocardium where the abnormally elongated cords rub. The agitation may also promote thrombus formation in the atrium.",True,Mitral Valve Prolapse (MVP),,,,
17adbb0f-b34b-4b8b-ac81-c2965657c362,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
17adbb0f-b34b-4b8b-ac81-c2965657c362,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
17adbb0f-b34b-4b8b-ac81-c2965657c362,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
17adbb0f-b34b-4b8b-ac81-c2965657c362,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
17adbb0f-b34b-4b8b-ac81-c2965657c362,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
17adbb0f-b34b-4b8b-ac81-c2965657c362,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
17adbb0f-b34b-4b8b-ac81-c2965657c362,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
38d5bdf6-3d11-49a9-bf9d-2479eda07e91,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,Rheumatic Heart Disease,False,Rheumatic Heart Disease,,,,
d7b6dd4b-dc30-4180-ae2b-4361e1372688,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Rheumatic heart disease (RHD) is virtually the only cause of mitral valve stenosis. It arises after a group A streptococcal infection that often originates in the upper airway and leads to rheumatic fever (a multisystem, immune-mediated disease). The incidence in developed countries is relatively low because of rapid diagnosis and treatment of the instigating pharyngitis, but in poor, crowed, urban areas RHD remains an important health issue.",True,Rheumatic Heart Disease,,,,
5100fb71-9a87-49cd-a64f-c3486971a939,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The acute results of rheumatic fever occur days to weeks after the streptococcal infection, and while the initial pharyngeal infection may have cleared and the test results have become negative, the antibodies to the streptococcal enzymes (Streptolysin O and DNase B) can still be detected. The initial cardiac effects include carditis, pericardial rubs, tachycardia, and arrhythmias. However, the chronic effects may arise years or even decades later.",True,Rheumatic Heart Disease,,,,
68f491d3-0d11-4083-b9f6-e14991fab7cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
68f491d3-0d11-4083-b9f6-e14991fab7cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
68f491d3-0d11-4083-b9f6-e14991fab7cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
68f491d3-0d11-4083-b9f6-e14991fab7cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
68f491d3-0d11-4083-b9f6-e14991fab7cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
68f491d3-0d11-4083-b9f6-e14991fab7cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
68f491d3-0d11-4083-b9f6-e14991fab7cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
46049816-79e6-4039-a442-26b4151bae22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
46049816-79e6-4039-a442-26b4151bae22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
46049816-79e6-4039-a442-26b4151bae22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
46049816-79e6-4039-a442-26b4151bae22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
46049816-79e6-4039-a442-26b4151bae22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
46049816-79e6-4039-a442-26b4151bae22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
46049816-79e6-4039-a442-26b4151bae22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
b5bbedc8-135f-4dbd-9015-b1558bb0a453,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,Infective Endocarditis,False,Infective Endocarditis,,,,
98294f4e-69a0-47d0-a244-afd8874bfa60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Infective endocarditis (IE) is divided into acute and subacute forms, depending on the virulence of the causal pathogen. Acute IE is rapid in onset and involves highly destructive pathogens that cause necrosis and significant lesions that can lead to death in a matter of days. Subacute IE, alternatively, can deform the valves over weeks to months and generally involves a much less destructive pathogen.",True,Infective Endocarditis,,,,
6fd1affb-ec0b-4df4-8d62-6ebfc4613f69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Acute cases tend to involve healthy individuals and are responsible for 20 to 30 percent of cases, whereas the less virulent pathogens that cause subacute IE tend to need a foothold and only affect previously damaged or deformed valves.",True,Infective Endocarditis,,,,
55cdcfb8-b806-48e9-86dc-b9551c1fdbca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
55cdcfb8-b806-48e9-86dc-b9551c1fdbca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
55cdcfb8-b806-48e9-86dc-b9551c1fdbca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
55cdcfb8-b806-48e9-86dc-b9551c1fdbca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
55cdcfb8-b806-48e9-86dc-b9551c1fdbca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
55cdcfb8-b806-48e9-86dc-b9551c1fdbca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
55cdcfb8-b806-48e9-86dc-b9551c1fdbca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
0f0822af-4ead-4cf2-9d1e-d11c4f82266f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,The risk is twofold as the vegetations can:,False,The risk is twofold as the vegetations can:,,,,
c04b8b0c-63a0-4617-81a5-374c7d3a1c3c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
c04b8b0c-63a0-4617-81a5-374c7d3a1c3c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
c04b8b0c-63a0-4617-81a5-374c7d3a1c3c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
c04b8b0c-63a0-4617-81a5-374c7d3a1c3c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
c04b8b0c-63a0-4617-81a5-374c7d3a1c3c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
c04b8b0c-63a0-4617-81a5-374c7d3a1c3c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
c04b8b0c-63a0-4617-81a5-374c7d3a1c3c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
c8aba7f0-f5dc-471e-9fce-74d90a4fcb72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,Noninfective Vegetations,False,Noninfective Vegetations,,,,
2aaa2137-4b4e-4075-91d3-7bbdb6a862bb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Some vegetations are sterile (i.e., occur in the absence of infection). There are two main examples of this—nonbacterial thrombotic endocarditis (NBTE) and the systemic lupus erythematosus (SLE).",True,Noninfective Vegetations,,,,
d01a4166-82f5-4385-b72f-44f94a8a8717,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
d01a4166-82f5-4385-b72f-44f94a8a8717,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
d01a4166-82f5-4385-b72f-44f94a8a8717,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
d01a4166-82f5-4385-b72f-44f94a8a8717,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
d01a4166-82f5-4385-b72f-44f94a8a8717,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
d01a4166-82f5-4385-b72f-44f94a8a8717,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
d01a4166-82f5-4385-b72f-44f94a8a8717,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
cbc9f3db-8fbf-42f5-9509-85ef16551527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
cbc9f3db-8fbf-42f5-9509-85ef16551527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
cbc9f3db-8fbf-42f5-9509-85ef16551527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
cbc9f3db-8fbf-42f5-9509-85ef16551527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
cbc9f3db-8fbf-42f5-9509-85ef16551527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
cbc9f3db-8fbf-42f5-9509-85ef16551527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
cbc9f3db-8fbf-42f5-9509-85ef16551527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
e34732da-90c0-4c51-934f-fbaa36e9b9bb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,Carcinoid Heart Disease,False,Carcinoid Heart Disease,,,,
3f32e131-37f5-4d91-8c3b-378a9802ddab,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
3f32e131-37f5-4d91-8c3b-378a9802ddab,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
3f32e131-37f5-4d91-8c3b-378a9802ddab,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
3f32e131-37f5-4d91-8c3b-378a9802ddab,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
3f32e131-37f5-4d91-8c3b-378a9802ddab,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
3f32e131-37f5-4d91-8c3b-378a9802ddab,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
3f32e131-37f5-4d91-8c3b-378a9802ddab,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
d6b5b9ea-de4b-4b29-afbb-300a262776a0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"The liver normally metabolizes these circulating mediators, but when the metastatic burden overwhelms hepatic clearance, the right heart is exposed to their effects (the left heart is somewhat protected by the degradation performed by the pulmonary circulation).",True,Carcinoid Heart Disease,,,,
34cd4033-6ae5-4c02-b9f0-6b6a08c444e8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
34cd4033-6ae5-4c02-b9f0-6b6a08c444e8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
34cd4033-6ae5-4c02-b9f0-6b6a08c444e8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
34cd4033-6ae5-4c02-b9f0-6b6a08c444e8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
34cd4033-6ae5-4c02-b9f0-6b6a08c444e8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
34cd4033-6ae5-4c02-b9f0-6b6a08c444e8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
34cd4033-6ae5-4c02-b9f0-6b6a08c444e8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
a1f28911-06a7-4d0f-b311-ea453ac8ff8f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,Text,False,Text,,,,
8ed007e3-fd33-4359-8d6e-b14888ccbed6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Dass, Clarissa, and Arun Kanmanthareddy. Rheumatic Heart Disease. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK538286/, CC BY 4.0.",True,Text,,,,
d95247e6-9a5a-4e0a-b269-04513578e66c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Douedi, Steven, and Hani Douedi. Mitral Regurgitation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK553135/, CC BY 4.0.",True,Text,,,,
589b8292-b0dc-48c9-9123-61d0eb189792,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Lopez, Diana M., Patrick T. O’Gara, and Leonard S. Lilly. “Valvular Heart  Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 8. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
d10b2c84-40d1-4da4-a723-dc238c00e3ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Wenn, Peter, and Roman Zeltser. Aortic Valve Disease. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK542205/, CC BY 4.0.",True,Text,,,,
4da1ad96-e7f7-4a38-9bc1-b475f2e3d609,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Infective Endocarditis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-4,"Table 4.1: Location of calcium deposits on aortic and mitral valves and their pathological consequences. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/4.2a_20220113",True,Text,,,,
ee41c323-71bf-49a1-b268-e3de89f0544d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Abnormalities of valvular structure and/or function can either be congenital or acquired. Acquired valvular disease is by far the most common and is most prevalent in the elderly. The high blood flow and pressures that valves are exposed to make them particularly susceptible to other risk factors that promote valvular damage (see table 4.1). Congenital valvular defects arise from disrupted heart development, about 50 percent of which involve the valves. The impact of congenital defects has diminished with the advent of advanced detection techniques. What we will spend time on in this chapter is the main instigating factors and pathologies that result in acquired valvular defects.",True,Text,,,,
564a7d52-2997-40d2-80e2-8e3975d93afc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,Table 4.1: Risk factors for acquired valvular damage.,True,Text,,,,
aa263a62-2d64-4f99-a461-db4af9e8785d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
aa263a62-2d64-4f99-a461-db4af9e8785d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
aa263a62-2d64-4f99-a461-db4af9e8785d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
aa263a62-2d64-4f99-a461-db4af9e8785d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
aa263a62-2d64-4f99-a461-db4af9e8785d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
aa263a62-2d64-4f99-a461-db4af9e8785d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
aa263a62-2d64-4f99-a461-db4af9e8785d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
00204ace-cd37-4bc4-b784-81a6fcfdb225,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"As they face the most pressure, the aortic and mitral valves are more prone to calcification. The most common pattern of calcification in the aortic valve is mounded masses within the cusps of the valve (see table 4.2) that eventually fuse and stop the valve from opening fully. Calcification in the mitral valve tends to start in the fibrous annulus, which does not impact valvular function to the same extent, but in exceptional cases can cause regurgitation or stenosis, or even arrhythmias as calcium deposits impinge on the atrioventricular conduction system (see table 4.2).",True,Text,,,,
afad9da4-d899-408e-b1c4-ae98d815d60a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,Table 4.2: Location of calcium deposits on aortic and mitral valves and their pathological consequences.,True,Text,,,,
d52364b4-44f2-4088-b41e-557781d95e7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,Mitral Valve Prolapse (MVP),False,Mitral Valve Prolapse (MVP),,,,
7302d9fe-edbc-4c3a-8235-8285629508e0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
7302d9fe-edbc-4c3a-8235-8285629508e0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
7302d9fe-edbc-4c3a-8235-8285629508e0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
7302d9fe-edbc-4c3a-8235-8285629508e0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
7302d9fe-edbc-4c3a-8235-8285629508e0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
7302d9fe-edbc-4c3a-8235-8285629508e0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
7302d9fe-edbc-4c3a-8235-8285629508e0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
d8413d40-b685-476c-8b15-9bb025b5f26e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The causes of MVP are usually unidentified, but a few cases can be attributed to inherited connective tissue disorders such as Marfan syndrome. The prolapsed valve leaflet composition is enlarged and thickened with deposition of myxomatous material rich in proteoglycans, and a reduction in the structurally critical fibrosa layer where a higher prevalence of type III collagen (a more stretchy than structural form of collagen) is found.",True,Mitral Valve Prolapse (MVP),,,,
dfca507e-a9d3-42f7-afe7-e12238688327,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The flapping valve structure can cause secondary fibrosis on the structures it strikes, such as the leaflet edges or the endocardium where the abnormally elongated cords rub. The agitation may also promote thrombus formation in the atrium.",True,Mitral Valve Prolapse (MVP),,,,
e352789f-e7d8-416f-ae5d-3ac811635612,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
e352789f-e7d8-416f-ae5d-3ac811635612,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
e352789f-e7d8-416f-ae5d-3ac811635612,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
e352789f-e7d8-416f-ae5d-3ac811635612,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
e352789f-e7d8-416f-ae5d-3ac811635612,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
e352789f-e7d8-416f-ae5d-3ac811635612,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
e352789f-e7d8-416f-ae5d-3ac811635612,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
d6e78e54-938d-4d2e-82a2-83b88b12fcfc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,Rheumatic Heart Disease,False,Rheumatic Heart Disease,,,,
173855a6-bb7c-4e93-9929-d7fb131d696a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Rheumatic heart disease (RHD) is virtually the only cause of mitral valve stenosis. It arises after a group A streptococcal infection that often originates in the upper airway and leads to rheumatic fever (a multisystem, immune-mediated disease). The incidence in developed countries is relatively low because of rapid diagnosis and treatment of the instigating pharyngitis, but in poor, crowed, urban areas RHD remains an important health issue.",True,Rheumatic Heart Disease,,,,
02bfa041-d2ba-472d-81ce-ccc200cccab9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The acute results of rheumatic fever occur days to weeks after the streptococcal infection, and while the initial pharyngeal infection may have cleared and the test results have become negative, the antibodies to the streptococcal enzymes (Streptolysin O and DNase B) can still be detected. The initial cardiac effects include carditis, pericardial rubs, tachycardia, and arrhythmias. However, the chronic effects may arise years or even decades later.",True,Rheumatic Heart Disease,,,,
bea73e72-b889-4d74-be28-8f212ee60f98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
bea73e72-b889-4d74-be28-8f212ee60f98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
bea73e72-b889-4d74-be28-8f212ee60f98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
bea73e72-b889-4d74-be28-8f212ee60f98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
bea73e72-b889-4d74-be28-8f212ee60f98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
bea73e72-b889-4d74-be28-8f212ee60f98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
bea73e72-b889-4d74-be28-8f212ee60f98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
3804996f-d641-4c0d-b7b9-54891162db5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
3804996f-d641-4c0d-b7b9-54891162db5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
3804996f-d641-4c0d-b7b9-54891162db5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
3804996f-d641-4c0d-b7b9-54891162db5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
3804996f-d641-4c0d-b7b9-54891162db5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
3804996f-d641-4c0d-b7b9-54891162db5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
3804996f-d641-4c0d-b7b9-54891162db5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
2f4d254c-58c5-4c0c-9d5a-120486bb843e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,Infective Endocarditis,False,Infective Endocarditis,,,,
c7880fa9-73e4-4328-9a17-97635cb14f9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Infective endocarditis (IE) is divided into acute and subacute forms, depending on the virulence of the causal pathogen. Acute IE is rapid in onset and involves highly destructive pathogens that cause necrosis and significant lesions that can lead to death in a matter of days. Subacute IE, alternatively, can deform the valves over weeks to months and generally involves a much less destructive pathogen.",True,Infective Endocarditis,,,,
9ab8891a-8180-4e35-a3da-31096b1f3e4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Acute cases tend to involve healthy individuals and are responsible for 20 to 30 percent of cases, whereas the less virulent pathogens that cause subacute IE tend to need a foothold and only affect previously damaged or deformed valves.",True,Infective Endocarditis,,,,
e1588d90-80a6-4228-a55f-1cab4954ea85,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
e1588d90-80a6-4228-a55f-1cab4954ea85,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
e1588d90-80a6-4228-a55f-1cab4954ea85,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
e1588d90-80a6-4228-a55f-1cab4954ea85,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
e1588d90-80a6-4228-a55f-1cab4954ea85,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
e1588d90-80a6-4228-a55f-1cab4954ea85,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
e1588d90-80a6-4228-a55f-1cab4954ea85,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
fb310a7a-68e1-4aa5-8894-e826e42709fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,The risk is twofold as the vegetations can:,False,The risk is twofold as the vegetations can:,,,,
553eb779-8e06-45d8-a54c-cedb66eddb23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
553eb779-8e06-45d8-a54c-cedb66eddb23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
553eb779-8e06-45d8-a54c-cedb66eddb23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
553eb779-8e06-45d8-a54c-cedb66eddb23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
553eb779-8e06-45d8-a54c-cedb66eddb23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
553eb779-8e06-45d8-a54c-cedb66eddb23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
553eb779-8e06-45d8-a54c-cedb66eddb23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
3847cf80-d827-44f0-9ba7-de583d861e09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,Noninfective Vegetations,False,Noninfective Vegetations,,,,
b5848d26-67e8-451d-877a-ec2119f93bab,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Some vegetations are sterile (i.e., occur in the absence of infection). There are two main examples of this—nonbacterial thrombotic endocarditis (NBTE) and the systemic lupus erythematosus (SLE).",True,Noninfective Vegetations,,,,
1199db57-91bb-43b1-9d54-3e329e0f4b95,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
1199db57-91bb-43b1-9d54-3e329e0f4b95,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
1199db57-91bb-43b1-9d54-3e329e0f4b95,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
1199db57-91bb-43b1-9d54-3e329e0f4b95,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
1199db57-91bb-43b1-9d54-3e329e0f4b95,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
1199db57-91bb-43b1-9d54-3e329e0f4b95,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
1199db57-91bb-43b1-9d54-3e329e0f4b95,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
73fdeb78-959b-4279-a135-3c234ad12c22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
73fdeb78-959b-4279-a135-3c234ad12c22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
73fdeb78-959b-4279-a135-3c234ad12c22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
73fdeb78-959b-4279-a135-3c234ad12c22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
73fdeb78-959b-4279-a135-3c234ad12c22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
73fdeb78-959b-4279-a135-3c234ad12c22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
73fdeb78-959b-4279-a135-3c234ad12c22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
a882ad38-c596-45ca-b0b0-2655f8f66505,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,Carcinoid Heart Disease,False,Carcinoid Heart Disease,,,,
71bdd666-06b8-4102-a746-7f17c77961a3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
71bdd666-06b8-4102-a746-7f17c77961a3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
71bdd666-06b8-4102-a746-7f17c77961a3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
71bdd666-06b8-4102-a746-7f17c77961a3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
71bdd666-06b8-4102-a746-7f17c77961a3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
71bdd666-06b8-4102-a746-7f17c77961a3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
71bdd666-06b8-4102-a746-7f17c77961a3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
b23eac95-aa26-4a11-b332-7bcbbafb5b0c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"The liver normally metabolizes these circulating mediators, but when the metastatic burden overwhelms hepatic clearance, the right heart is exposed to their effects (the left heart is somewhat protected by the degradation performed by the pulmonary circulation).",True,Carcinoid Heart Disease,,,,
6cde3adf-6acf-4135-a122-f261a91ff852,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
6cde3adf-6acf-4135-a122-f261a91ff852,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
6cde3adf-6acf-4135-a122-f261a91ff852,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
6cde3adf-6acf-4135-a122-f261a91ff852,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
6cde3adf-6acf-4135-a122-f261a91ff852,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
6cde3adf-6acf-4135-a122-f261a91ff852,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
6cde3adf-6acf-4135-a122-f261a91ff852,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
f9704688-0b57-4305-aa67-60a89f9d93da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,Text,False,Text,,,,
306e2668-5275-4e1f-a50b-2b872b20548d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Dass, Clarissa, and Arun Kanmanthareddy. Rheumatic Heart Disease. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK538286/, CC BY 4.0.",True,Text,,,,
90fb87a0-9f4d-45a4-94dc-07f15db69893,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Douedi, Steven, and Hani Douedi. Mitral Regurgitation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK553135/, CC BY 4.0.",True,Text,,,,
b346f9e4-2fc6-4642-a9ea-bd7aaf2028fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Lopez, Diana M., Patrick T. O’Gara, and Leonard S. Lilly. “Valvular Heart  Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 8. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
d3c532f4-47b1-4ca4-85cd-6af8d2ba9ed7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Wenn, Peter, and Roman Zeltser. Aortic Valve Disease. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK542205/, CC BY 4.0.",True,Text,,,,
1681f876-c85e-472e-bb3a-da721f3f786c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-3,"Table 4.1: Location of calcium deposits on aortic and mitral valves and their pathological consequences. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/4.2a_20220113",True,Text,,,,
ad8b1b70-a454-45f1-ae43-60b72e3b943e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Abnormalities of valvular structure and/or function can either be congenital or acquired. Acquired valvular disease is by far the most common and is most prevalent in the elderly. The high blood flow and pressures that valves are exposed to make them particularly susceptible to other risk factors that promote valvular damage (see table 4.1). Congenital valvular defects arise from disrupted heart development, about 50 percent of which involve the valves. The impact of congenital defects has diminished with the advent of advanced detection techniques. What we will spend time on in this chapter is the main instigating factors and pathologies that result in acquired valvular defects.",True,Text,,,,
45077798-2970-4756-ba23-9ab2a0e5fdf8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,Table 4.1: Risk factors for acquired valvular damage.,True,Text,,,,
5d5a294e-1e85-4ced-b45a-f0a1d4a647e9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
5d5a294e-1e85-4ced-b45a-f0a1d4a647e9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
5d5a294e-1e85-4ced-b45a-f0a1d4a647e9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
5d5a294e-1e85-4ced-b45a-f0a1d4a647e9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
5d5a294e-1e85-4ced-b45a-f0a1d4a647e9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
5d5a294e-1e85-4ced-b45a-f0a1d4a647e9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
5d5a294e-1e85-4ced-b45a-f0a1d4a647e9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
4ce985fb-8ea6-430e-8f9c-051b21d43829,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"As they face the most pressure, the aortic and mitral valves are more prone to calcification. The most common pattern of calcification in the aortic valve is mounded masses within the cusps of the valve (see table 4.2) that eventually fuse and stop the valve from opening fully. Calcification in the mitral valve tends to start in the fibrous annulus, which does not impact valvular function to the same extent, but in exceptional cases can cause regurgitation or stenosis, or even arrhythmias as calcium deposits impinge on the atrioventricular conduction system (see table 4.2).",True,Text,,,,
108f1afd-d9e5-4cd9-bcca-3c088b811c83,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,Table 4.2: Location of calcium deposits on aortic and mitral valves and their pathological consequences.,True,Text,,,,
79477466-8f82-40ae-a225-a6439e6f57f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,Mitral Valve Prolapse (MVP),False,Mitral Valve Prolapse (MVP),,,,
d4110bd3-4f5c-436e-a5a1-ddecf891d80d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
d4110bd3-4f5c-436e-a5a1-ddecf891d80d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
d4110bd3-4f5c-436e-a5a1-ddecf891d80d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
d4110bd3-4f5c-436e-a5a1-ddecf891d80d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
d4110bd3-4f5c-436e-a5a1-ddecf891d80d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
d4110bd3-4f5c-436e-a5a1-ddecf891d80d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
d4110bd3-4f5c-436e-a5a1-ddecf891d80d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
821eeea3-ab70-4021-bc17-8652f53d6f39,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The causes of MVP are usually unidentified, but a few cases can be attributed to inherited connective tissue disorders such as Marfan syndrome. The prolapsed valve leaflet composition is enlarged and thickened with deposition of myxomatous material rich in proteoglycans, and a reduction in the structurally critical fibrosa layer where a higher prevalence of type III collagen (a more stretchy than structural form of collagen) is found.",True,Mitral Valve Prolapse (MVP),,,,
6cb402fa-1bf7-44c8-921e-3da814332c9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The flapping valve structure can cause secondary fibrosis on the structures it strikes, such as the leaflet edges or the endocardium where the abnormally elongated cords rub. The agitation may also promote thrombus formation in the atrium.",True,Mitral Valve Prolapse (MVP),,,,
f9988eab-9a91-4caf-85ab-1c486535fcb5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
f9988eab-9a91-4caf-85ab-1c486535fcb5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
f9988eab-9a91-4caf-85ab-1c486535fcb5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
f9988eab-9a91-4caf-85ab-1c486535fcb5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
f9988eab-9a91-4caf-85ab-1c486535fcb5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
f9988eab-9a91-4caf-85ab-1c486535fcb5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
f9988eab-9a91-4caf-85ab-1c486535fcb5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
cbae304f-293f-47f2-b1e2-842060e0a8c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,Rheumatic Heart Disease,False,Rheumatic Heart Disease,,,,
1ce8c1b8-0d47-4961-962a-354e12ab748f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Rheumatic heart disease (RHD) is virtually the only cause of mitral valve stenosis. It arises after a group A streptococcal infection that often originates in the upper airway and leads to rheumatic fever (a multisystem, immune-mediated disease). The incidence in developed countries is relatively low because of rapid diagnosis and treatment of the instigating pharyngitis, but in poor, crowed, urban areas RHD remains an important health issue.",True,Rheumatic Heart Disease,,,,
117a9622-8417-4922-b536-2dc288cb8f28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The acute results of rheumatic fever occur days to weeks after the streptococcal infection, and while the initial pharyngeal infection may have cleared and the test results have become negative, the antibodies to the streptococcal enzymes (Streptolysin O and DNase B) can still be detected. The initial cardiac effects include carditis, pericardial rubs, tachycardia, and arrhythmias. However, the chronic effects may arise years or even decades later.",True,Rheumatic Heart Disease,,,,
a65f9838-05ea-4b9e-8002-ee1ecd276cbe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
a65f9838-05ea-4b9e-8002-ee1ecd276cbe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
a65f9838-05ea-4b9e-8002-ee1ecd276cbe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
a65f9838-05ea-4b9e-8002-ee1ecd276cbe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
a65f9838-05ea-4b9e-8002-ee1ecd276cbe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
a65f9838-05ea-4b9e-8002-ee1ecd276cbe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
a65f9838-05ea-4b9e-8002-ee1ecd276cbe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
74fdd72a-d54a-4367-9b17-5bf90672db5d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
74fdd72a-d54a-4367-9b17-5bf90672db5d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
74fdd72a-d54a-4367-9b17-5bf90672db5d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
74fdd72a-d54a-4367-9b17-5bf90672db5d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
74fdd72a-d54a-4367-9b17-5bf90672db5d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
74fdd72a-d54a-4367-9b17-5bf90672db5d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
74fdd72a-d54a-4367-9b17-5bf90672db5d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
253b3330-43d0-41aa-85b1-2a8503be597b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,Infective Endocarditis,False,Infective Endocarditis,,,,
1bdc8aff-fe56-4f2b-a783-72943e72b47b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Infective endocarditis (IE) is divided into acute and subacute forms, depending on the virulence of the causal pathogen. Acute IE is rapid in onset and involves highly destructive pathogens that cause necrosis and significant lesions that can lead to death in a matter of days. Subacute IE, alternatively, can deform the valves over weeks to months and generally involves a much less destructive pathogen.",True,Infective Endocarditis,,,,
dd202ec2-2c9c-433f-ba1b-6bdca4923dcc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Acute cases tend to involve healthy individuals and are responsible for 20 to 30 percent of cases, whereas the less virulent pathogens that cause subacute IE tend to need a foothold and only affect previously damaged or deformed valves.",True,Infective Endocarditis,,,,
04fc9c1f-3186-4d7c-9496-4093da6be757,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
04fc9c1f-3186-4d7c-9496-4093da6be757,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
04fc9c1f-3186-4d7c-9496-4093da6be757,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
04fc9c1f-3186-4d7c-9496-4093da6be757,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
04fc9c1f-3186-4d7c-9496-4093da6be757,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
04fc9c1f-3186-4d7c-9496-4093da6be757,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
04fc9c1f-3186-4d7c-9496-4093da6be757,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
9443081e-9b78-4a2d-af33-ab3677afcfd0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,The risk is twofold as the vegetations can:,False,The risk is twofold as the vegetations can:,,,,
5bf72181-5c4c-408a-9d72-e69abbbf05b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
5bf72181-5c4c-408a-9d72-e69abbbf05b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
5bf72181-5c4c-408a-9d72-e69abbbf05b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
5bf72181-5c4c-408a-9d72-e69abbbf05b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
5bf72181-5c4c-408a-9d72-e69abbbf05b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
5bf72181-5c4c-408a-9d72-e69abbbf05b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
5bf72181-5c4c-408a-9d72-e69abbbf05b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
58361d07-d1ff-4285-8490-132ebb1a5893,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,Noninfective Vegetations,False,Noninfective Vegetations,,,,
c06e2667-b118-44c6-9fe6-364ba2bc3e58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Some vegetations are sterile (i.e., occur in the absence of infection). There are two main examples of this—nonbacterial thrombotic endocarditis (NBTE) and the systemic lupus erythematosus (SLE).",True,Noninfective Vegetations,,,,
451a7ddf-9b70-4e39-9f0f-edb8be63d192,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
451a7ddf-9b70-4e39-9f0f-edb8be63d192,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
451a7ddf-9b70-4e39-9f0f-edb8be63d192,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
451a7ddf-9b70-4e39-9f0f-edb8be63d192,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
451a7ddf-9b70-4e39-9f0f-edb8be63d192,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
451a7ddf-9b70-4e39-9f0f-edb8be63d192,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
451a7ddf-9b70-4e39-9f0f-edb8be63d192,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
ad8cc086-eeb5-4a5c-986c-1e3a9f20fcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
ad8cc086-eeb5-4a5c-986c-1e3a9f20fcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
ad8cc086-eeb5-4a5c-986c-1e3a9f20fcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
ad8cc086-eeb5-4a5c-986c-1e3a9f20fcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
ad8cc086-eeb5-4a5c-986c-1e3a9f20fcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
ad8cc086-eeb5-4a5c-986c-1e3a9f20fcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
ad8cc086-eeb5-4a5c-986c-1e3a9f20fcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
dcef448e-9d8b-41c3-a070-1287f588615f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,Carcinoid Heart Disease,False,Carcinoid Heart Disease,,,,
9ab951c9-37ca-42bf-b300-2f728b32966f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
9ab951c9-37ca-42bf-b300-2f728b32966f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
9ab951c9-37ca-42bf-b300-2f728b32966f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
9ab951c9-37ca-42bf-b300-2f728b32966f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
9ab951c9-37ca-42bf-b300-2f728b32966f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
9ab951c9-37ca-42bf-b300-2f728b32966f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
9ab951c9-37ca-42bf-b300-2f728b32966f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
313d36ee-633d-40fd-9b44-ddec9c86eeb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"The liver normally metabolizes these circulating mediators, but when the metastatic burden overwhelms hepatic clearance, the right heart is exposed to their effects (the left heart is somewhat protected by the degradation performed by the pulmonary circulation).",True,Carcinoid Heart Disease,,,,
ec999f66-7bde-464d-b434-593317b7f156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
ec999f66-7bde-464d-b434-593317b7f156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
ec999f66-7bde-464d-b434-593317b7f156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
ec999f66-7bde-464d-b434-593317b7f156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
ec999f66-7bde-464d-b434-593317b7f156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
ec999f66-7bde-464d-b434-593317b7f156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
ec999f66-7bde-464d-b434-593317b7f156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
853098b8-7877-476d-9a4b-eff35b41d2f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,Text,False,Text,,,,
c0b94e73-6e33-4dc1-8292-83f0c7050741,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Dass, Clarissa, and Arun Kanmanthareddy. Rheumatic Heart Disease. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK538286/, CC BY 4.0.",True,Text,,,,
0b1b33a0-0aa3-4952-8d05-c29916427985,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Douedi, Steven, and Hani Douedi. Mitral Regurgitation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK553135/, CC BY 4.0.",True,Text,,,,
fb2015e4-3e19-4e27-8dba-583b174909c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Lopez, Diana M., Patrick T. O’Gara, and Leonard S. Lilly. “Valvular Heart  Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 8. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
3fde6d44-694a-4ba0-8840-d73382f99253,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Wenn, Peter, and Roman Zeltser. Aortic Valve Disease. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK542205/, CC BY 4.0.",True,Text,,,,
5962ae15-57b2-4569-8c92-e251106ebe8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-2,"Table 4.1: Location of calcium deposits on aortic and mitral valves and their pathological consequences. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/4.2a_20220113",True,Text,,,,
a9f8f27a-9d32-4725-9a81-e34177655fe6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Abnormalities of valvular structure and/or function can either be congenital or acquired. Acquired valvular disease is by far the most common and is most prevalent in the elderly. The high blood flow and pressures that valves are exposed to make them particularly susceptible to other risk factors that promote valvular damage (see table 4.1). Congenital valvular defects arise from disrupted heart development, about 50 percent of which involve the valves. The impact of congenital defects has diminished with the advent of advanced detection techniques. What we will spend time on in this chapter is the main instigating factors and pathologies that result in acquired valvular defects.",True,Text,,,,
2d839490-958b-4ec8-ac90-4ee5e55fb4e8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,Table 4.1: Risk factors for acquired valvular damage.,True,Text,,,,
1a74ecc2-7b40-46cd-ad3a-d7ce384da5f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
1a74ecc2-7b40-46cd-ad3a-d7ce384da5f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
1a74ecc2-7b40-46cd-ad3a-d7ce384da5f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
1a74ecc2-7b40-46cd-ad3a-d7ce384da5f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
1a74ecc2-7b40-46cd-ad3a-d7ce384da5f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
1a74ecc2-7b40-46cd-ad3a-d7ce384da5f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
1a74ecc2-7b40-46cd-ad3a-d7ce384da5f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
548aeb71-80a5-4829-886e-ac9c22b76dab,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"As they face the most pressure, the aortic and mitral valves are more prone to calcification. The most common pattern of calcification in the aortic valve is mounded masses within the cusps of the valve (see table 4.2) that eventually fuse and stop the valve from opening fully. Calcification in the mitral valve tends to start in the fibrous annulus, which does not impact valvular function to the same extent, but in exceptional cases can cause regurgitation or stenosis, or even arrhythmias as calcium deposits impinge on the atrioventricular conduction system (see table 4.2).",True,Text,,,,
75ae18da-d254-454d-827a-0be2b94d7f66,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,Table 4.2: Location of calcium deposits on aortic and mitral valves and their pathological consequences.,True,Text,,,,
b708da0a-3ab9-42a7-8d8f-78822b3f1121,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,Mitral Valve Prolapse (MVP),False,Mitral Valve Prolapse (MVP),,,,
f36dab46-28b2-4eb5-8e84-fac122abd218,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
f36dab46-28b2-4eb5-8e84-fac122abd218,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
f36dab46-28b2-4eb5-8e84-fac122abd218,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
f36dab46-28b2-4eb5-8e84-fac122abd218,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
f36dab46-28b2-4eb5-8e84-fac122abd218,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
f36dab46-28b2-4eb5-8e84-fac122abd218,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
f36dab46-28b2-4eb5-8e84-fac122abd218,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
ac36295d-f11d-4a0c-a292-bd5c3e164c28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The causes of MVP are usually unidentified, but a few cases can be attributed to inherited connective tissue disorders such as Marfan syndrome. The prolapsed valve leaflet composition is enlarged and thickened with deposition of myxomatous material rich in proteoglycans, and a reduction in the structurally critical fibrosa layer where a higher prevalence of type III collagen (a more stretchy than structural form of collagen) is found.",True,Mitral Valve Prolapse (MVP),,,,
68849176-f846-4384-a332-885c7a6933e8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The flapping valve structure can cause secondary fibrosis on the structures it strikes, such as the leaflet edges or the endocardium where the abnormally elongated cords rub. The agitation may also promote thrombus formation in the atrium.",True,Mitral Valve Prolapse (MVP),,,,
c031d6b3-e5ad-4de0-94b6-47bc11bf2562,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
c031d6b3-e5ad-4de0-94b6-47bc11bf2562,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
c031d6b3-e5ad-4de0-94b6-47bc11bf2562,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
c031d6b3-e5ad-4de0-94b6-47bc11bf2562,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
c031d6b3-e5ad-4de0-94b6-47bc11bf2562,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
c031d6b3-e5ad-4de0-94b6-47bc11bf2562,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
c031d6b3-e5ad-4de0-94b6-47bc11bf2562,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
ac1ad6cc-fc3a-41de-a88c-949038cbeefc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,Rheumatic Heart Disease,False,Rheumatic Heart Disease,,,,
b4924422-48b8-4df8-b10f-002c597af63a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Rheumatic heart disease (RHD) is virtually the only cause of mitral valve stenosis. It arises after a group A streptococcal infection that often originates in the upper airway and leads to rheumatic fever (a multisystem, immune-mediated disease). The incidence in developed countries is relatively low because of rapid diagnosis and treatment of the instigating pharyngitis, but in poor, crowed, urban areas RHD remains an important health issue.",True,Rheumatic Heart Disease,,,,
29768c4b-931d-4cca-9f96-9a67642a224d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The acute results of rheumatic fever occur days to weeks after the streptococcal infection, and while the initial pharyngeal infection may have cleared and the test results have become negative, the antibodies to the streptococcal enzymes (Streptolysin O and DNase B) can still be detected. The initial cardiac effects include carditis, pericardial rubs, tachycardia, and arrhythmias. However, the chronic effects may arise years or even decades later.",True,Rheumatic Heart Disease,,,,
4f8ab559-0d09-48ed-a204-e426ff174563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
4f8ab559-0d09-48ed-a204-e426ff174563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
4f8ab559-0d09-48ed-a204-e426ff174563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
4f8ab559-0d09-48ed-a204-e426ff174563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
4f8ab559-0d09-48ed-a204-e426ff174563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
4f8ab559-0d09-48ed-a204-e426ff174563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
4f8ab559-0d09-48ed-a204-e426ff174563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
da026886-e6ed-4cee-a1b4-f46bc7a5085e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
da026886-e6ed-4cee-a1b4-f46bc7a5085e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
da026886-e6ed-4cee-a1b4-f46bc7a5085e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
da026886-e6ed-4cee-a1b4-f46bc7a5085e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
da026886-e6ed-4cee-a1b4-f46bc7a5085e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
da026886-e6ed-4cee-a1b4-f46bc7a5085e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
da026886-e6ed-4cee-a1b4-f46bc7a5085e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
301203bd-5e65-41ce-9ff7-f6b6a3595757,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,Infective Endocarditis,False,Infective Endocarditis,,,,
568f7c6b-9858-47d4-b7ee-baad16cd41eb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Infective endocarditis (IE) is divided into acute and subacute forms, depending on the virulence of the causal pathogen. Acute IE is rapid in onset and involves highly destructive pathogens that cause necrosis and significant lesions that can lead to death in a matter of days. Subacute IE, alternatively, can deform the valves over weeks to months and generally involves a much less destructive pathogen.",True,Infective Endocarditis,,,,
1d7ca4ec-f3fa-476f-913e-79e9d73ec476,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Acute cases tend to involve healthy individuals and are responsible for 20 to 30 percent of cases, whereas the less virulent pathogens that cause subacute IE tend to need a foothold and only affect previously damaged or deformed valves.",True,Infective Endocarditis,,,,
ade93ffd-544b-4caf-9f65-4cb249ea9cc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
ade93ffd-544b-4caf-9f65-4cb249ea9cc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
ade93ffd-544b-4caf-9f65-4cb249ea9cc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
ade93ffd-544b-4caf-9f65-4cb249ea9cc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
ade93ffd-544b-4caf-9f65-4cb249ea9cc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
ade93ffd-544b-4caf-9f65-4cb249ea9cc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
ade93ffd-544b-4caf-9f65-4cb249ea9cc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
b62d8dc8-5f34-4bc5-9550-04421c23ccdb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,The risk is twofold as the vegetations can:,False,The risk is twofold as the vegetations can:,,,,
644d8f3b-c2dc-49d3-a000-7bc10c8ceede,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
644d8f3b-c2dc-49d3-a000-7bc10c8ceede,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
644d8f3b-c2dc-49d3-a000-7bc10c8ceede,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
644d8f3b-c2dc-49d3-a000-7bc10c8ceede,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
644d8f3b-c2dc-49d3-a000-7bc10c8ceede,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
644d8f3b-c2dc-49d3-a000-7bc10c8ceede,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
644d8f3b-c2dc-49d3-a000-7bc10c8ceede,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
db1e371d-dead-4632-a163-15f75b8d9a26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,Noninfective Vegetations,False,Noninfective Vegetations,,,,
72051c4e-f1d5-4169-ba28-dc53b8470bbf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Some vegetations are sterile (i.e., occur in the absence of infection). There are two main examples of this—nonbacterial thrombotic endocarditis (NBTE) and the systemic lupus erythematosus (SLE).",True,Noninfective Vegetations,,,,
b3565a53-0e54-4073-862e-296e1b3c11ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
b3565a53-0e54-4073-862e-296e1b3c11ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
b3565a53-0e54-4073-862e-296e1b3c11ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
b3565a53-0e54-4073-862e-296e1b3c11ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
b3565a53-0e54-4073-862e-296e1b3c11ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
b3565a53-0e54-4073-862e-296e1b3c11ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
b3565a53-0e54-4073-862e-296e1b3c11ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
bab4a890-003f-4a06-8ba3-8321419af18c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
bab4a890-003f-4a06-8ba3-8321419af18c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
bab4a890-003f-4a06-8ba3-8321419af18c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
bab4a890-003f-4a06-8ba3-8321419af18c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
bab4a890-003f-4a06-8ba3-8321419af18c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
bab4a890-003f-4a06-8ba3-8321419af18c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
bab4a890-003f-4a06-8ba3-8321419af18c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
ebed6069-a18a-4444-bd11-7de59d822e10,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,Carcinoid Heart Disease,False,Carcinoid Heart Disease,,,,
ccf20ab8-9837-49bf-8f1d-caa93a64bec1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
ccf20ab8-9837-49bf-8f1d-caa93a64bec1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
ccf20ab8-9837-49bf-8f1d-caa93a64bec1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
ccf20ab8-9837-49bf-8f1d-caa93a64bec1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
ccf20ab8-9837-49bf-8f1d-caa93a64bec1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
ccf20ab8-9837-49bf-8f1d-caa93a64bec1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
ccf20ab8-9837-49bf-8f1d-caa93a64bec1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
46d758a9-110f-43ce-b36d-6e6ce924ba2a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"The liver normally metabolizes these circulating mediators, but when the metastatic burden overwhelms hepatic clearance, the right heart is exposed to their effects (the left heart is somewhat protected by the degradation performed by the pulmonary circulation).",True,Carcinoid Heart Disease,,,,
3f75d0f4-f8eb-4389-b1a1-00bd0539a28e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
3f75d0f4-f8eb-4389-b1a1-00bd0539a28e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
3f75d0f4-f8eb-4389-b1a1-00bd0539a28e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
3f75d0f4-f8eb-4389-b1a1-00bd0539a28e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
3f75d0f4-f8eb-4389-b1a1-00bd0539a28e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
3f75d0f4-f8eb-4389-b1a1-00bd0539a28e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
3f75d0f4-f8eb-4389-b1a1-00bd0539a28e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
6c270ce4-204f-4d05-b701-cfac5fb97bae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,Text,False,Text,,,,
a268f422-ae39-42e1-868e-2fb6dd636527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Dass, Clarissa, and Arun Kanmanthareddy. Rheumatic Heart Disease. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK538286/, CC BY 4.0.",True,Text,,,,
7e913ade-37a5-494d-b917-7e4424afd904,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Douedi, Steven, and Hani Douedi. Mitral Regurgitation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK553135/, CC BY 4.0.",True,Text,,,,
8c5703cc-8605-472b-811f-ce5284b4e610,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Lopez, Diana M., Patrick T. O’Gara, and Leonard S. Lilly. “Valvular Heart  Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 8. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
d5cdc69d-5101-4bfd-932f-fe113f9fba74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Wenn, Peter, and Roman Zeltser. Aortic Valve Disease. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK542205/, CC BY 4.0.",True,Text,,,,
569cdcb1-4101-4049-ad98-fc3fb1a8882b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/#chapter-36-section-1,"Table 4.1: Location of calcium deposits on aortic and mitral valves and their pathological consequences. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/4.2a_20220113",True,Text,,,,
d6ef21b4-b230-43c6-8c41-2c224100f829,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Abnormalities of valvular structure and/or function can either be congenital or acquired. Acquired valvular disease is by far the most common and is most prevalent in the elderly. The high blood flow and pressures that valves are exposed to make them particularly susceptible to other risk factors that promote valvular damage (see table 4.1). Congenital valvular defects arise from disrupted heart development, about 50 percent of which involve the valves. The impact of congenital defects has diminished with the advent of advanced detection techniques. What we will spend time on in this chapter is the main instigating factors and pathologies that result in acquired valvular defects.",True,Text,,,,
a2fad5d9-6dd6-407e-9d88-607d175d5701,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,Table 4.1: Risk factors for acquired valvular damage.,True,Text,,,,
d5771b10-0382-40c8-8fc0-3f6c6739e758,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
d5771b10-0382-40c8-8fc0-3f6c6739e758,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
d5771b10-0382-40c8-8fc0-3f6c6739e758,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
d5771b10-0382-40c8-8fc0-3f6c6739e758,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
d5771b10-0382-40c8-8fc0-3f6c6739e758,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
d5771b10-0382-40c8-8fc0-3f6c6739e758,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
d5771b10-0382-40c8-8fc0-3f6c6739e758,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences, and the most common valvular disorder is calcification that comes with “wear-and-tear” and aging. The presence of other factors such as hyperlipidemia, hypertension, and inflammation accelerate this process and promote the deposition of hydroxyapatite (a form of calcium phosphate), and the valve structure contains cells that resemble osteoblasts (figure 4.1).",True,Text,Figure 4.1,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.1-new.jpg,Figure 4.1: Histological view of the ossification of valve tissue with osteoblast-like cells clustered in the center of the field of view. These cells are responsible for the calcification and consequent stiffening of the valve leaflet.
07ee80ae-0ef8-4976-ad21-f3aff9481b97,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"As they face the most pressure, the aortic and mitral valves are more prone to calcification. The most common pattern of calcification in the aortic valve is mounded masses within the cusps of the valve (see table 4.2) that eventually fuse and stop the valve from opening fully. Calcification in the mitral valve tends to start in the fibrous annulus, which does not impact valvular function to the same extent, but in exceptional cases can cause regurgitation or stenosis, or even arrhythmias as calcium deposits impinge on the atrioventricular conduction system (see table 4.2).",True,Text,,,,
f8513000-559e-4cf7-8fce-c20b80f1917a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,Table 4.2: Location of calcium deposits on aortic and mitral valves and their pathological consequences.,True,Text,,,,
56ef699d-f1a8-490a-b03d-6f5022962a5d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,Mitral Valve Prolapse (MVP),False,Mitral Valve Prolapse (MVP),,,,
035126ac-14c8-43c8-b284-1b61a5ea7a79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
035126ac-14c8-43c8-b284-1b61a5ea7a79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
035126ac-14c8-43c8-b284-1b61a5ea7a79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
035126ac-14c8-43c8-b284-1b61a5ea7a79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
035126ac-14c8-43c8-b284-1b61a5ea7a79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
035126ac-14c8-43c8-b284-1b61a5ea7a79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
035126ac-14c8-43c8-b284-1b61a5ea7a79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"A prolapsed mitral valve is one where one or both leaflets have become floppy and capable of ballooning back into the left atrium during systole (figure 4.2). The condition is more common in women, affects 2–3 percent of adults in the United States, and can be a secondary effect of mitral valve regurgitation.",True,Mitral Valve Prolapse (MVP),Figure 4.2,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
c4cc7b09-71a9-4b83-a2a7-f298108f2e55,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The causes of MVP are usually unidentified, but a few cases can be attributed to inherited connective tissue disorders such as Marfan syndrome. The prolapsed valve leaflet composition is enlarged and thickened with deposition of myxomatous material rich in proteoglycans, and a reduction in the structurally critical fibrosa layer where a higher prevalence of type III collagen (a more stretchy than structural form of collagen) is found.",True,Mitral Valve Prolapse (MVP),,,,
e83ebe83-27e4-4104-af08-f41f3dd29ef4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The flapping valve structure can cause secondary fibrosis on the structures it strikes, such as the leaflet edges or the endocardium where the abnormally elongated cords rub. The agitation may also promote thrombus formation in the atrium.",True,Mitral Valve Prolapse (MVP),,,,
31eb67f6-e8f0-49fb-af34-add521575674,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
31eb67f6-e8f0-49fb-af34-add521575674,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
31eb67f6-e8f0-49fb-af34-add521575674,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
31eb67f6-e8f0-49fb-af34-add521575674,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
31eb67f6-e8f0-49fb-af34-add521575674,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
31eb67f6-e8f0-49fb-af34-add521575674,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
31eb67f6-e8f0-49fb-af34-add521575674,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The resultant floppy leaflet can be detected by a midsystolic click, and any associated incompetence may produce a late-systolic murmur (summary in figure 4.2). MVP is usually asymptomatic, but potential complications include:",True,Mitral Valve Prolapse (MVP),Figure 4.2,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.2-new-scaled.jpg,Figure 4.2: Mitral valve prolapse.
ec1a110d-863b-4aa3-a38c-d2ce85ee308a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,Rheumatic Heart Disease,False,Rheumatic Heart Disease,,,,
283effa7-d329-4de2-9f0c-d59303592e8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Rheumatic heart disease (RHD) is virtually the only cause of mitral valve stenosis. It arises after a group A streptococcal infection that often originates in the upper airway and leads to rheumatic fever (a multisystem, immune-mediated disease). The incidence in developed countries is relatively low because of rapid diagnosis and treatment of the instigating pharyngitis, but in poor, crowed, urban areas RHD remains an important health issue.",True,Rheumatic Heart Disease,,,,
f325fbf9-d89f-4581-ac66-e8d0565ef1c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The acute results of rheumatic fever occur days to weeks after the streptococcal infection, and while the initial pharyngeal infection may have cleared and the test results have become negative, the antibodies to the streptococcal enzymes (Streptolysin O and DNase B) can still be detected. The initial cardiac effects include carditis, pericardial rubs, tachycardia, and arrhythmias. However, the chronic effects may arise years or even decades later.",True,Rheumatic Heart Disease,,,,
06551bf1-b8c4-4aa2-aa38-186add688c9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
06551bf1-b8c4-4aa2-aa38-186add688c9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
06551bf1-b8c4-4aa2-aa38-186add688c9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
06551bf1-b8c4-4aa2-aa38-186add688c9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
06551bf1-b8c4-4aa2-aa38-186add688c9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
06551bf1-b8c4-4aa2-aa38-186add688c9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
06551bf1-b8c4-4aa2-aa38-186add688c9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The chronic effects involve an immune cross-reaction between the antibodies and CD4+ T-cells directed against the streptococcal M proteins and cardiac self-antigens. Antibody binding and T-cell activity toward the cardiac antigens activate complement and recruit neutrophils and macrophages toward the valve tissue. The damage they produce includes histologically distinct lesions called Aschoff bodies (figure 4.3), and plump activated macrophages called Anitschkow cells (or caterpillar cells) appear in the effected areas (figure 4.3). All layers of the myocardium can be effected, but the valves can show leaflet thickening and fusion as well as shortened, thickened cords. Vegetative verrucae are associated with the necrotic fibrinoid foci, making RHD one of the vegetative forms of valvular disease.",True,Rheumatic Heart Disease,Figure 4.3,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
8cc9dd33-d642-4603-b5dc-bb2ac9888320,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
8cc9dd33-d642-4603-b5dc-bb2ac9888320,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
8cc9dd33-d642-4603-b5dc-bb2ac9888320,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
8cc9dd33-d642-4603-b5dc-bb2ac9888320,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
8cc9dd33-d642-4603-b5dc-bb2ac9888320,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
8cc9dd33-d642-4603-b5dc-bb2ac9888320,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
8cc9dd33-d642-4603-b5dc-bb2ac9888320,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"As the valve thickens it can become calcified as well, and the adhered leaflets produce a “fish-mouth” or “button hole” appearance  that causes the valve to narrow. The damage is cumulative with the increased turbulence through a stenosed valve perpetuating the fibrotic process (see summary in figure 4.3).",True,Rheumatic Heart Disease,Figure 4.3,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.3-scaled.jpg,Figure 4.3: Pathophysiology of rheumatic heart disease.
558cd53c-c36f-4c41-ad89-da5a0645238d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,Infective Endocarditis,False,Infective Endocarditis,,,,
a614d491-8587-4333-b3ec-f59f9ccff19f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Infective endocarditis (IE) is divided into acute and subacute forms, depending on the virulence of the causal pathogen. Acute IE is rapid in onset and involves highly destructive pathogens that cause necrosis and significant lesions that can lead to death in a matter of days. Subacute IE, alternatively, can deform the valves over weeks to months and generally involves a much less destructive pathogen.",True,Infective Endocarditis,,,,
c252a8ac-6395-4aa2-8b41-2ba491b3b7b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Acute cases tend to involve healthy individuals and are responsible for 20 to 30 percent of cases, whereas the less virulent pathogens that cause subacute IE tend to need a foothold and only affect previously damaged or deformed valves.",True,Infective Endocarditis,,,,
f2f6c592-13a3-4cf7-8118-dc8b11c5880a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
f2f6c592-13a3-4cf7-8118-dc8b11c5880a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
f2f6c592-13a3-4cf7-8118-dc8b11c5880a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
f2f6c592-13a3-4cf7-8118-dc8b11c5880a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
f2f6c592-13a3-4cf7-8118-dc8b11c5880a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
f2f6c592-13a3-4cf7-8118-dc8b11c5880a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
f2f6c592-13a3-4cf7-8118-dc8b11c5880a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Most incidence of IE start with fever, but it can also manifest as nonspecific fatigue, weight loss, or flu-like symptoms in older adults. The infection leads to vegetations on the valve that are the hallmark of IE (figure 4.4). These lesions contain fibrin, inflammatory cells, and bacteria.",True,Infective Endocarditis,Figure 4.4,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.4-scaled.jpg,Figure 4.4: Vegetative lesions (in white box) associated with IE.
607ca8ac-b755-41b4-9cf0-bb135c47b8e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,The risk is twofold as the vegetations can:,False,The risk is twofold as the vegetations can:,,,,
ddf1acb8-31ff-4e49-bc03-bf646274a44b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
ddf1acb8-31ff-4e49-bc03-bf646274a44b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
ddf1acb8-31ff-4e49-bc03-bf646274a44b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
ddf1acb8-31ff-4e49-bc03-bf646274a44b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
ddf1acb8-31ff-4e49-bc03-bf646274a44b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
ddf1acb8-31ff-4e49-bc03-bf646274a44b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
ddf1acb8-31ff-4e49-bc03-bf646274a44b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"After a few weeks, complications arise that are the product of immune complex deposition or emboli. They can include glomerulonephritis as immune complexes become embedded in the glomerular basement membrane. Other later complications are now rare due to early detection and effective treatment but can include microthromboemboli that produce splinter or subungual lesions. Other hemorrhagic signs include Janeway lesions on the palms or soles, Osler nodes on the fingers, or Roth spots on the retina (figure 4.5).",True,The risk is twofold as the vegetations can:,Figure 4.5,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.6-scaled.jpg,"Figure 4.5: Signs of IE include Janeway lesions (left), Osler nodes (middle), and Roth spots (right)."
3bebedbb-0bfd-43b8-9bd7-636011ad13e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,Noninfective Vegetations,False,Noninfective Vegetations,,,,
1afbb16f-58e6-4c44-bdb7-8c5c0b4e2760,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Some vegetations are sterile (i.e., occur in the absence of infection). There are two main examples of this—nonbacterial thrombotic endocarditis (NBTE) and the systemic lupus erythematosus (SLE).",True,Noninfective Vegetations,,,,
32dd452f-7340-42f9-8710-052988487e22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
32dd452f-7340-42f9-8710-052988487e22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
32dd452f-7340-42f9-8710-052988487e22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
32dd452f-7340-42f9-8710-052988487e22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
32dd452f-7340-42f9-8710-052988487e22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
32dd452f-7340-42f9-8710-052988487e22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
32dd452f-7340-42f9-8710-052988487e22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Often coinciding with emboli in other sites, NBTE occurs in states of hypercoagulability, such as in cancer or sepsis. The small thrombi (1–5 mm) bind to the valve leaflets (figure 4.6), but do not illicit an inflammatory response nor are they invasive. Often the local consequences are trivial, but they can be the source of emboli that lead to infarcts in the brain, heart, or elsewhere.",True,Noninfective Vegetations,Figure 4.6,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.7-pic.jpeg,Figure 4.6: NBTE with small thrombi binding to valve leaflets.
dd6fb542-07f5-4151-a0d4-dc5c56243864,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
dd6fb542-07f5-4151-a0d4-dc5c56243864,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
dd6fb542-07f5-4151-a0d4-dc5c56243864,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
dd6fb542-07f5-4151-a0d4-dc5c56243864,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
dd6fb542-07f5-4151-a0d4-dc5c56243864,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
dd6fb542-07f5-4151-a0d4-dc5c56243864,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
dd6fb542-07f5-4151-a0d4-dc5c56243864,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"In SLE, the vegetations are again sterile and small (1–4 mm) with a pink, wart-like appearance that are composed of eosinophilic material, granular material, and cellular debris. They tend to adhere to the undersurfaces of the atrioventricular valves, the valvular endocardium, and the cords (figure 4.7). Unlike NBTE, the vegetations can instigate complement and Fc-bearing cells that cause intense valvulitis. The end product of this is referred to as Libman Sacks disease.",True,Noninfective Vegetations,Figure 4.7,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.8.jpeg,Figure 4.7: Small “wart-like vegetations” in the cords of a valve.
745d736e-f61a-4832-98fe-57c964813ac4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,Carcinoid Heart Disease,False,Carcinoid Heart Disease,,,,
b1fde884-0b80-46ce-95c1-0e9858f44b3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
b1fde884-0b80-46ce-95c1-0e9858f44b3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
b1fde884-0b80-46ce-95c1-0e9858f44b3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
b1fde884-0b80-46ce-95c1-0e9858f44b3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
b1fde884-0b80-46ce-95c1-0e9858f44b3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
b1fde884-0b80-46ce-95c1-0e9858f44b3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
b1fde884-0b80-46ce-95c1-0e9858f44b3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Lastly, carcinoid heart disease is the cardiac manifestation of carcinoid syndrome. Carcinoid tumors are neuroendocrine tumors that usually arise in the gastrointestinal tract or lungs, and they secrete a number of mediators (figure 4.8) that can give rise to carcinoid heart disease.",True,Carcinoid Heart Disease,Figure 4.8,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
f1f6473d-4685-4075-81a9-c726f60c7781,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"The liver normally metabolizes these circulating mediators, but when the metastatic burden overwhelms hepatic clearance, the right heart is exposed to their effects (the left heart is somewhat protected by the degradation performed by the pulmonary circulation).",True,Carcinoid Heart Disease,,,,
bc943f2f-7f3a-4925-a6bc-a5edfd112c2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Carcinoid Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
bc943f2f-7f3a-4925-a6bc-a5edfd112c2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Noninfective Vegetations,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
bc943f2f-7f3a-4925-a6bc-a5edfd112c2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Infective Endocarditis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
bc943f2f-7f3a-4925-a6bc-a5edfd112c2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Rheumatic Heart Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
bc943f2f-7f3a-4925-a6bc-a5edfd112c2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Mitral Valve Prolapse (MVP),https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
bc943f2f-7f3a-4925-a6bc-a5edfd112c2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,Pathophysiology of Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
bc943f2f-7f3a-4925-a6bc-a5edfd112c2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Of all these released mediators, serotonin is the most likely candidate for causing cardiac effects, although the mechanism is not clear. Once established, carcinoid lesions are distinctive white intimal thickenings (figure 4.8) composed of smooth muscle cells and collagen embedded in a mucopolysaccharide matrix. The most common manifestations are tricuspid insufficiency and pulmonary stenosis.",True,Carcinoid Heart Disease,Figure 4.8,4. Valvular Disease,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/4.9.png,Figure 4.8: Release of inflammatory mediators from neuroendocrine tumors leading to carcinoid heart disease.
02db04e8-2d66-4044-9c5f-162eb682a14f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,Text,False,Text,,,,
1ab9f47e-e06d-4e26-9581-33a938c5c0b9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Dass, Clarissa, and Arun Kanmanthareddy. Rheumatic Heart Disease. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK538286/, CC BY 4.0.",True,Text,,,,
6a342c2c-9738-4c80-a531-14dff9ed512f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Douedi, Steven, and Hani Douedi. Mitral Regurgitation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK553135/, CC BY 4.0.",True,Text,,,,
fb496c0f-00ab-410b-ad3f-41ba344fbf1f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Lopez, Diana M., Patrick T. O’Gara, and Leonard S. Lilly. “Valvular Heart  Disease.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 8. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
8a59044c-f77a-498a-a92d-4374b95dfbda,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Wenn, Peter, and Roman Zeltser. Aortic Valve Disease. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK542205/, CC BY 4.0.",True,Text,,,,
1a2f83a2-4dc0-416d-aaed-0cdcf0255703,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,4. Valvular Disease,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-4-valvular-disease/,"Table 4.1: Location of calcium deposits on aortic and mitral valves and their pathological consequences. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/4.2a_20220113",True,Text,,,,
36cfa87f-cb4a-40da-be59-3fe09efefb82,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"The current guidelines (JNC 8, 2017) list the following pressures and categories to define hypertension:",True,Text,,,,
ca95c35a-0b57-45d0-9703-1d6bb256020a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,JNC,False,JNC,,,,
17c3cb39-d548-4da3-b59e-211a3acb1f40,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,Hypertensive Crisis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
17c3cb39-d548-4da3-b59e-211a3acb1f40,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,Consequences of Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
17c3cb39-d548-4da3-b59e-211a3acb1f40,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,Secondary Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
17c3cb39-d548-4da3-b59e-211a3acb1f40,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,Essential Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
17c3cb39-d548-4da3-b59e-211a3acb1f40,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,3. Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
bd8f6ac2-ffb9-44cd-b02f-17ae00fcf21a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,Genetic components of essential hypertension,False,Genetic components of essential hypertension,,,,
4184d91a-cb44-49b4-bcbc-cdd7b0e4adff,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"No single loci has been identified as causing hypertension, but strong familial histories suggest polygenic causes (i.e., multiple loci are involved). Much attention has been paid to genes involved with enzymes and receptor production within the Renin-Angiotensin-Aldosterone (RAA) system because of its critical role in blood pressure control through sodium and volume regulation. Similarly genes involved with renal regulation of sodium have been studied. Our inability to demonstrate a genetic basis to hypertension is also consistent with significant environmental causes.",True,Genetic components of essential hypertension,,,,
b7e052e3-654a-4a17-87a7-6db87f0f5912,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,Systemic abnormalities and EH,False,Systemic abnormalities and EH,,,,
ade4db08-4c80-4062-a00a-d762ac4f1a0f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,Hypertensive Crisis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
ade4db08-4c80-4062-a00a-d762ac4f1a0f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,Consequences of Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
ade4db08-4c80-4062-a00a-d762ac4f1a0f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,Secondary Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
ade4db08-4c80-4062-a00a-d762ac4f1a0f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,Essential Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
ade4db08-4c80-4062-a00a-d762ac4f1a0f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,3. Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
c3b6d65d-b3fa-495f-9a7c-8e790f15aac0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"Diabetes, obesity, and EH",False,"Diabetes, obesity, and EH",,,,
d3b69c04-1d15-4424-af89-f77f1666b7c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"The linkage between diabetes and EH, and obesity and EH, appears strong and direct. Because insulin is a dietary-induced mediator of sympathetic activity, the elevated insulin levels in insulin-resistant diabetes can directly promote hypertension. Insulin can also lead to an increase in peripheral resistance via its mitogenic effect on vascular smooth muscle that causes hypertrophy in the medial vascular layers and a decrease in lumen size.",True,"Diabetes, obesity, and EH",,,,
0aa43dbb-2668-4efb-a242-208f5a95abc7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"Obesity can also induce hypertension through release of angiotensinogen from more abundant adipocytes, thus providing more substrate for the RAA system. The increase in body mass is also accompanied by an increase in blood volume, and that blood may be more viscous as the large population of adipocytes release coagulative proteins, including prothrombin.",True,"Diabetes, obesity, and EH",,,,
75060c42-4a07-43bd-b3d8-76a55bb39a88,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,Secondary Hypertension,False,Secondary Hypertension,,,,
2668fb3a-6fdd-45e9-8cf6-051e1d037aa6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"Although not as common, there are numerous causes of secondary hypertension. There are some distinguishing features that are clinically useful to distinguish it from EH. Your first heads-up is if the patient is younger and not in the typical range for EH (> fifty years old). Secondary hypertension also tends to be more severe, and BP can rise dramatically; EH does not have a rapid onset. While EH often comes with family history, secondary hypertension is more sporadic.",True,Secondary Hypertension,,,,
c91ed7c1-a706-4945-a2c5-4c0b8a9b5695,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"Suspicion of secondary hypertension can usually be confirmed by urinalysis that reveals the underlying issue (see table 3.1 for some common causes and cues for diagnosis). Disturbances in electrolytes and creatinine accompany the renal and mineralocorticoid-based diseases. Pheochromocytoma is rare and accounts for 0.2 percent of secondary hypertension cases (however, it is much more common in exam questions than it is in the clinic!).",True,Secondary Hypertension,,,,
54d3be50-bfae-46a9-a39c-282c93b69103,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"Drugs that disrupt the angiotensinogen pathways (e.g., estrogens), are sympathomimetic (e.g., over-the-counter cold remedies), or promote sodium and water retention (e.g., NSAIDS) can all produce secondary hypertension.",True,Secondary Hypertension,,,,
8d5e0d50-b1e4-47bb-bee9-8a863d69af60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,Consequences of Hypertension,False,Consequences of Hypertension,,,,
af882988-7ccc-462e-9505-98fd0bd3263c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"As most hypertensive patients are asymptomatic, the condition can be left unmanaged and allowed to produce significant chronic effects. Most of these effects are caused by the extra work placed on the heart with the increased afterload and the damage to the interior of the vasculature.",True,Consequences of Hypertension,,,,
d283f412-2185-450b-9f1e-c9490be56efa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"The excess afterload can lead to systolic dysfunction and eventually heart failure with reduced ejection fraction (HFREF). In response to the excessive afterload the left ventricle can hypertrophy, causing a loss of compliance diastolic dysfunction and eventually heart failure with normal ejection fraction (HFNEF). The increased workload and muscle mass also increase the myocardial oxygen demand. This increase in demand often occurs at the same time that blood supply is diminished by concurrent atherosclerosis that is accelerated by the hypertension-induced arterial damage. Consequently, with high demand and low supply, the patient is prone to ischemia and myocardial infarction.",True,Consequences of Hypertension,,,,
c1ed34a9-7d84-4ac5-9417-1199bdbf9872,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"The arterial damage will also promote thrombosis and atheroemboli, so risk of embolic stroke is raised. Risk of hemorrhagic stroke is also increased as the vessel ways become weak. The large vessels are also at risk of being unable to counteract raised pressure (remember Laplace’s law?), so aortic aneurysm and dissection can also occur.",True,Consequences of Hypertension,,,,
a8286b9f-39dc-4ddd-a8c6-737c69993a46,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"High pressures entering the renal circulation can lead to nephrosclerosis. As renal function declines, a vicious cycle forms with renal failure exacerbating hypertension that exacerbates renal failure.",True,Consequences of Hypertension,,,,
020ddd29-fe19-4942-a12e-51cb278a5826,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,Hypertensive Crisis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
020ddd29-fe19-4942-a12e-51cb278a5826,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,Consequences of Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
020ddd29-fe19-4942-a12e-51cb278a5826,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,Secondary Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
020ddd29-fe19-4942-a12e-51cb278a5826,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,Essential Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
020ddd29-fe19-4942-a12e-51cb278a5826,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,3. Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
96a5472c-9338-4294-b65a-0fdb83b57265,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,Hypertensive Crisis,False,Hypertensive Crisis,,,,
73d9b885-aa84-4b56-81a7-5ed3c181505c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"Most commonly caused by a hemodynamic insult overlaid on chronic hypertension, a hypertensive crisis is a severe elevation of blood pressure that can become life threatening through raising intracranial pressure. The rise in intracranial pressure produces severe headache, blurred vision, confusion, or even coma and is referred to as hypertensive encephalopathy. Funduscopy reveals retinal hemorrhages, exudates, and sometimes papilledema. The massive afterload on the left ventricle can precipitate angina. Therapy must be rapid to prevent permanent vascular consequences, and if administered in time the acute changes are usually reversed. However, the underlying cause of the crisis (usually renal failure) will persist.",True,Hypertensive Crisis,,,,
77f1820e-39b5-4c07-b4d0-7efbd1decc68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,Text,False,Text,,,,
043d0a6c-c109-49d3-864d-1049ae0bab92,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"Brown, Jenifer M., Gordon H. Williams, and Leonard S. Lilly. “Hypertension.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 13. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
6a1b6fe6-83fe-406c-9e01-1a06a4791350,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"Hajar, Rachel. “Framingham Contribution to Cardiovascular Disease.” Heart Views 17, no. 2 (April–June 2016): 78–81. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4966216.",True,Text,,,,
b09e6339-ed87-40ae-b475-924c98e1a575,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"Iqbal, Arshad Muhammad, and Syed F. Jaml. Essential Hypertension. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK539859/, CC BY 4.0.",True,Text,,,,
df8f6825-cd8d-4f33-a3b6-3aa95e2b7231,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hypertensive Crisis,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-4,"Page, Michael R. “The JNC 8 Hypertension Guidelines: An In-Depth Guide.” Evidence-Based Diabetes Management 20, no. SP1  (January 2014). https://www.ajmc.com/view/the-jnc-8-hypertension-guidelines-an-in-depth-guide.",True,Text,,,,
24512123-f7e2-472e-beb1-0da22af8a29d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"The current guidelines (JNC 8, 2017) list the following pressures and categories to define hypertension:",True,Text,,,,
20fa8fc3-a3f5-426e-b728-c2e97086c116,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,JNC,False,JNC,,,,
cd306069-ab94-4730-ba29-3f20d2c2ef40,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,Hypertensive Crisis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
cd306069-ab94-4730-ba29-3f20d2c2ef40,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,Consequences of Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
cd306069-ab94-4730-ba29-3f20d2c2ef40,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,Secondary Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
cd306069-ab94-4730-ba29-3f20d2c2ef40,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,Essential Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
cd306069-ab94-4730-ba29-3f20d2c2ef40,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,3. Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
0cfd0716-01f7-4547-bf4e-4a83ab74a43d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,Genetic components of essential hypertension,False,Genetic components of essential hypertension,,,,
cbc29abb-6917-4247-b939-9fcd8481793c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"No single loci has been identified as causing hypertension, but strong familial histories suggest polygenic causes (i.e., multiple loci are involved). Much attention has been paid to genes involved with enzymes and receptor production within the Renin-Angiotensin-Aldosterone (RAA) system because of its critical role in blood pressure control through sodium and volume regulation. Similarly genes involved with renal regulation of sodium have been studied. Our inability to demonstrate a genetic basis to hypertension is also consistent with significant environmental causes.",True,Genetic components of essential hypertension,,,,
b7c09f1c-fa3c-4bae-b75a-8f01c3121f6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,Systemic abnormalities and EH,False,Systemic abnormalities and EH,,,,
c215a0de-d22d-462f-914c-acfe568419df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,Hypertensive Crisis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
c215a0de-d22d-462f-914c-acfe568419df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,Consequences of Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
c215a0de-d22d-462f-914c-acfe568419df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,Secondary Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
c215a0de-d22d-462f-914c-acfe568419df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,Essential Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
c215a0de-d22d-462f-914c-acfe568419df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,3. Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
0d30f652-843d-48d3-b2ab-9d80574f7db5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"Diabetes, obesity, and EH",False,"Diabetes, obesity, and EH",,,,
19c3da44-8c63-406a-9d0f-e06e3c5aec24,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"The linkage between diabetes and EH, and obesity and EH, appears strong and direct. Because insulin is a dietary-induced mediator of sympathetic activity, the elevated insulin levels in insulin-resistant diabetes can directly promote hypertension. Insulin can also lead to an increase in peripheral resistance via its mitogenic effect on vascular smooth muscle that causes hypertrophy in the medial vascular layers and a decrease in lumen size.",True,"Diabetes, obesity, and EH",,,,
d5917741-2165-427f-9ce8-29da9872233e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"Obesity can also induce hypertension through release of angiotensinogen from more abundant adipocytes, thus providing more substrate for the RAA system. The increase in body mass is also accompanied by an increase in blood volume, and that blood may be more viscous as the large population of adipocytes release coagulative proteins, including prothrombin.",True,"Diabetes, obesity, and EH",,,,
8dd19b7c-4fb1-4377-a2a0-02df27e3c4b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,Secondary Hypertension,False,Secondary Hypertension,,,,
c59ea62b-6743-4108-a79e-d9dd1cd12817,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"Although not as common, there are numerous causes of secondary hypertension. There are some distinguishing features that are clinically useful to distinguish it from EH. Your first heads-up is if the patient is younger and not in the typical range for EH (> fifty years old). Secondary hypertension also tends to be more severe, and BP can rise dramatically; EH does not have a rapid onset. While EH often comes with family history, secondary hypertension is more sporadic.",True,Secondary Hypertension,,,,
ddf20199-7f5a-49de-a1a3-3366331bba56,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"Suspicion of secondary hypertension can usually be confirmed by urinalysis that reveals the underlying issue (see table 3.1 for some common causes and cues for diagnosis). Disturbances in electrolytes and creatinine accompany the renal and mineralocorticoid-based diseases. Pheochromocytoma is rare and accounts for 0.2 percent of secondary hypertension cases (however, it is much more common in exam questions than it is in the clinic!).",True,Secondary Hypertension,,,,
133fa251-1ed0-4f80-a32c-bbb67ae6ebd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"Drugs that disrupt the angiotensinogen pathways (e.g., estrogens), are sympathomimetic (e.g., over-the-counter cold remedies), or promote sodium and water retention (e.g., NSAIDS) can all produce secondary hypertension.",True,Secondary Hypertension,,,,
048055b0-2667-4db8-b0ca-8fffd3c6c5ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,Consequences of Hypertension,False,Consequences of Hypertension,,,,
0a8c54fb-f180-4926-84f8-8f88a5503f3c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"As most hypertensive patients are asymptomatic, the condition can be left unmanaged and allowed to produce significant chronic effects. Most of these effects are caused by the extra work placed on the heart with the increased afterload and the damage to the interior of the vasculature.",True,Consequences of Hypertension,,,,
ad304ec3-3dd1-429a-9469-c0054227dc57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"The excess afterload can lead to systolic dysfunction and eventually heart failure with reduced ejection fraction (HFREF). In response to the excessive afterload the left ventricle can hypertrophy, causing a loss of compliance diastolic dysfunction and eventually heart failure with normal ejection fraction (HFNEF). The increased workload and muscle mass also increase the myocardial oxygen demand. This increase in demand often occurs at the same time that blood supply is diminished by concurrent atherosclerosis that is accelerated by the hypertension-induced arterial damage. Consequently, with high demand and low supply, the patient is prone to ischemia and myocardial infarction.",True,Consequences of Hypertension,,,,
bc8b1a7e-782b-4485-8422-f41e4734d0c1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"The arterial damage will also promote thrombosis and atheroemboli, so risk of embolic stroke is raised. Risk of hemorrhagic stroke is also increased as the vessel ways become weak. The large vessels are also at risk of being unable to counteract raised pressure (remember Laplace’s law?), so aortic aneurysm and dissection can also occur.",True,Consequences of Hypertension,,,,
1e7aeb79-d4ed-4f36-9a0b-79341ad9b833,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"High pressures entering the renal circulation can lead to nephrosclerosis. As renal function declines, a vicious cycle forms with renal failure exacerbating hypertension that exacerbates renal failure.",True,Consequences of Hypertension,,,,
c552c2b0-9af9-4930-b481-bc1346e493bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,Hypertensive Crisis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
c552c2b0-9af9-4930-b481-bc1346e493bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,Consequences of Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
c552c2b0-9af9-4930-b481-bc1346e493bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,Secondary Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
c552c2b0-9af9-4930-b481-bc1346e493bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,Essential Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
c552c2b0-9af9-4930-b481-bc1346e493bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,3. Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
525d0af7-d8d3-40f7-af60-5db0b5d13aa1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,Hypertensive Crisis,False,Hypertensive Crisis,,,,
18954875-270d-416b-a162-46272f6dff99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"Most commonly caused by a hemodynamic insult overlaid on chronic hypertension, a hypertensive crisis is a severe elevation of blood pressure that can become life threatening through raising intracranial pressure. The rise in intracranial pressure produces severe headache, blurred vision, confusion, or even coma and is referred to as hypertensive encephalopathy. Funduscopy reveals retinal hemorrhages, exudates, and sometimes papilledema. The massive afterload on the left ventricle can precipitate angina. Therapy must be rapid to prevent permanent vascular consequences, and if administered in time the acute changes are usually reversed. However, the underlying cause of the crisis (usually renal failure) will persist.",True,Hypertensive Crisis,,,,
88318167-6bef-4a36-a38c-6eadfc93747c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,Text,False,Text,,,,
a7cb2523-d9a8-4b2f-aa45-593f9fc626ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"Brown, Jenifer M., Gordon H. Williams, and Leonard S. Lilly. “Hypertension.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 13. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
b855d30b-5747-464c-b5a3-39fcd5e1ca5f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"Hajar, Rachel. “Framingham Contribution to Cardiovascular Disease.” Heart Views 17, no. 2 (April–June 2016): 78–81. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4966216.",True,Text,,,,
c5139191-4ebd-4f49-8b7a-3d233f3f36c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"Iqbal, Arshad Muhammad, and Syed F. Jaml. Essential Hypertension. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK539859/, CC BY 4.0.",True,Text,,,,
87402944-a06f-4c07-ac59-f36f4f3057c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Consequences of Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-3,"Page, Michael R. “The JNC 8 Hypertension Guidelines: An In-Depth Guide.” Evidence-Based Diabetes Management 20, no. SP1  (January 2014). https://www.ajmc.com/view/the-jnc-8-hypertension-guidelines-an-in-depth-guide.",True,Text,,,,
fb777a00-54cc-4084-ad02-5839a10879e8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"The current guidelines (JNC 8, 2017) list the following pressures and categories to define hypertension:",True,Text,,,,
9e13d95a-08c1-4290-97ac-8b05306c6968,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,JNC,False,JNC,,,,
9bf3cb16-7c01-42a3-833a-bd4a218ce440,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,Hypertensive Crisis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
9bf3cb16-7c01-42a3-833a-bd4a218ce440,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,Consequences of Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
9bf3cb16-7c01-42a3-833a-bd4a218ce440,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,Secondary Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
9bf3cb16-7c01-42a3-833a-bd4a218ce440,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,Essential Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
9bf3cb16-7c01-42a3-833a-bd4a218ce440,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,3. Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
4cba5662-cb4f-4ab7-870e-024fd5b3b25c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,Genetic components of essential hypertension,False,Genetic components of essential hypertension,,,,
a43f7fc2-103a-4d5c-a923-f68328e65f6e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"No single loci has been identified as causing hypertension, but strong familial histories suggest polygenic causes (i.e., multiple loci are involved). Much attention has been paid to genes involved with enzymes and receptor production within the Renin-Angiotensin-Aldosterone (RAA) system because of its critical role in blood pressure control through sodium and volume regulation. Similarly genes involved with renal regulation of sodium have been studied. Our inability to demonstrate a genetic basis to hypertension is also consistent with significant environmental causes.",True,Genetic components of essential hypertension,,,,
489f8ff0-0b41-4955-801d-12836c816ef5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,Systemic abnormalities and EH,False,Systemic abnormalities and EH,,,,
f4c5c50e-47f3-40ce-a9da-7853833fdf26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,Hypertensive Crisis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
f4c5c50e-47f3-40ce-a9da-7853833fdf26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,Consequences of Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
f4c5c50e-47f3-40ce-a9da-7853833fdf26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,Secondary Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
f4c5c50e-47f3-40ce-a9da-7853833fdf26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,Essential Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
f4c5c50e-47f3-40ce-a9da-7853833fdf26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,3. Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
b18cd764-b65a-4563-ba7a-8f211c4bd4e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"Diabetes, obesity, and EH",False,"Diabetes, obesity, and EH",,,,
b6be3a28-1a9b-4325-9898-96a29205947d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"The linkage between diabetes and EH, and obesity and EH, appears strong and direct. Because insulin is a dietary-induced mediator of sympathetic activity, the elevated insulin levels in insulin-resistant diabetes can directly promote hypertension. Insulin can also lead to an increase in peripheral resistance via its mitogenic effect on vascular smooth muscle that causes hypertrophy in the medial vascular layers and a decrease in lumen size.",True,"Diabetes, obesity, and EH",,,,
e056131a-6b79-41c7-9b31-5cc5fe3dad6c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"Obesity can also induce hypertension through release of angiotensinogen from more abundant adipocytes, thus providing more substrate for the RAA system. The increase in body mass is also accompanied by an increase in blood volume, and that blood may be more viscous as the large population of adipocytes release coagulative proteins, including prothrombin.",True,"Diabetes, obesity, and EH",,,,
4f0d53b9-74d5-4ac6-919b-2012ef7549d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,Secondary Hypertension,False,Secondary Hypertension,,,,
6294e2d4-caeb-41ed-a6c3-bc6539710dce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"Although not as common, there are numerous causes of secondary hypertension. There are some distinguishing features that are clinically useful to distinguish it from EH. Your first heads-up is if the patient is younger and not in the typical range for EH (> fifty years old). Secondary hypertension also tends to be more severe, and BP can rise dramatically; EH does not have a rapid onset. While EH often comes with family history, secondary hypertension is more sporadic.",True,Secondary Hypertension,,,,
321744e9-2334-40d2-ae98-7c66fd7e582a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"Suspicion of secondary hypertension can usually be confirmed by urinalysis that reveals the underlying issue (see table 3.1 for some common causes and cues for diagnosis). Disturbances in electrolytes and creatinine accompany the renal and mineralocorticoid-based diseases. Pheochromocytoma is rare and accounts for 0.2 percent of secondary hypertension cases (however, it is much more common in exam questions than it is in the clinic!).",True,Secondary Hypertension,,,,
66b856d5-d674-4172-8990-0b5c0f05f501,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"Drugs that disrupt the angiotensinogen pathways (e.g., estrogens), are sympathomimetic (e.g., over-the-counter cold remedies), or promote sodium and water retention (e.g., NSAIDS) can all produce secondary hypertension.",True,Secondary Hypertension,,,,
a13bd1f4-a70a-4f1c-b187-11727c692bb5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,Consequences of Hypertension,False,Consequences of Hypertension,,,,
f70eb491-2e1c-42ca-9ea8-07c86961074a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"As most hypertensive patients are asymptomatic, the condition can be left unmanaged and allowed to produce significant chronic effects. Most of these effects are caused by the extra work placed on the heart with the increased afterload and the damage to the interior of the vasculature.",True,Consequences of Hypertension,,,,
85429ea2-ee89-447f-b34f-5797fbb5da18,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"The excess afterload can lead to systolic dysfunction and eventually heart failure with reduced ejection fraction (HFREF). In response to the excessive afterload the left ventricle can hypertrophy, causing a loss of compliance diastolic dysfunction and eventually heart failure with normal ejection fraction (HFNEF). The increased workload and muscle mass also increase the myocardial oxygen demand. This increase in demand often occurs at the same time that blood supply is diminished by concurrent atherosclerosis that is accelerated by the hypertension-induced arterial damage. Consequently, with high demand and low supply, the patient is prone to ischemia and myocardial infarction.",True,Consequences of Hypertension,,,,
da343b0d-6f1b-4f71-bce1-477524d74bce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"The arterial damage will also promote thrombosis and atheroemboli, so risk of embolic stroke is raised. Risk of hemorrhagic stroke is also increased as the vessel ways become weak. The large vessels are also at risk of being unable to counteract raised pressure (remember Laplace’s law?), so aortic aneurysm and dissection can also occur.",True,Consequences of Hypertension,,,,
6f2c3de4-63ee-4bec-93b8-b693eaa94f71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"High pressures entering the renal circulation can lead to nephrosclerosis. As renal function declines, a vicious cycle forms with renal failure exacerbating hypertension that exacerbates renal failure.",True,Consequences of Hypertension,,,,
0b182756-c30a-4df3-9954-cbbe18123ee0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,Hypertensive Crisis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
0b182756-c30a-4df3-9954-cbbe18123ee0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,Consequences of Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
0b182756-c30a-4df3-9954-cbbe18123ee0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,Secondary Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
0b182756-c30a-4df3-9954-cbbe18123ee0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,Essential Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
0b182756-c30a-4df3-9954-cbbe18123ee0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,3. Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
40795f63-38aa-4992-aab0-e69352a1e13a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,Hypertensive Crisis,False,Hypertensive Crisis,,,,
920ea264-cc6a-405c-9bee-b6da12afe047,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"Most commonly caused by a hemodynamic insult overlaid on chronic hypertension, a hypertensive crisis is a severe elevation of blood pressure that can become life threatening through raising intracranial pressure. The rise in intracranial pressure produces severe headache, blurred vision, confusion, or even coma and is referred to as hypertensive encephalopathy. Funduscopy reveals retinal hemorrhages, exudates, and sometimes papilledema. The massive afterload on the left ventricle can precipitate angina. Therapy must be rapid to prevent permanent vascular consequences, and if administered in time the acute changes are usually reversed. However, the underlying cause of the crisis (usually renal failure) will persist.",True,Hypertensive Crisis,,,,
b7393bcb-1516-45c9-bf27-daa5d4156547,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,Text,False,Text,,,,
489004fd-86a0-4e02-bcb9-42f33bd1a293,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"Brown, Jenifer M., Gordon H. Williams, and Leonard S. Lilly. “Hypertension.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 13. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
2da3d998-f834-4e0c-8da8-6a4632e7fd7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"Hajar, Rachel. “Framingham Contribution to Cardiovascular Disease.” Heart Views 17, no. 2 (April–June 2016): 78–81. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4966216.",True,Text,,,,
75828dc0-6001-4bcd-a95a-e014a88956cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"Iqbal, Arshad Muhammad, and Syed F. Jaml. Essential Hypertension. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK539859/, CC BY 4.0.",True,Text,,,,
b8fa95c6-3e68-4a3a-8f11-daeca0e44219,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Secondary Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-2,"Page, Michael R. “The JNC 8 Hypertension Guidelines: An In-Depth Guide.” Evidence-Based Diabetes Management 20, no. SP1  (January 2014). https://www.ajmc.com/view/the-jnc-8-hypertension-guidelines-an-in-depth-guide.",True,Text,,,,
b391e501-f6a5-4dff-b2c3-6008c505227c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"The current guidelines (JNC 8, 2017) list the following pressures and categories to define hypertension:",True,Text,,,,
66bfa6e8-075a-4476-9ad6-6a70cbca430e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,JNC,False,JNC,,,,
24d24c8f-c834-4a65-99b4-c94a203598bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,Hypertensive Crisis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
24d24c8f-c834-4a65-99b4-c94a203598bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,Consequences of Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
24d24c8f-c834-4a65-99b4-c94a203598bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,Secondary Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
24d24c8f-c834-4a65-99b4-c94a203598bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,Essential Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
24d24c8f-c834-4a65-99b4-c94a203598bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,3. Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
3fef1e9b-88f7-4d43-8a51-af594145a5e8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,Genetic components of essential hypertension,False,Genetic components of essential hypertension,,,,
2e547aaa-59ad-4380-9bbd-702176e5ab5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"No single loci has been identified as causing hypertension, but strong familial histories suggest polygenic causes (i.e., multiple loci are involved). Much attention has been paid to genes involved with enzymes and receptor production within the Renin-Angiotensin-Aldosterone (RAA) system because of its critical role in blood pressure control through sodium and volume regulation. Similarly genes involved with renal regulation of sodium have been studied. Our inability to demonstrate a genetic basis to hypertension is also consistent with significant environmental causes.",True,Genetic components of essential hypertension,,,,
0b9a74fa-2273-462b-a72f-e9b646e18f20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,Systemic abnormalities and EH,False,Systemic abnormalities and EH,,,,
8e0180a4-bea1-4d44-923f-e3755da77bec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,Hypertensive Crisis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
8e0180a4-bea1-4d44-923f-e3755da77bec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,Consequences of Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
8e0180a4-bea1-4d44-923f-e3755da77bec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,Secondary Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
8e0180a4-bea1-4d44-923f-e3755da77bec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,Essential Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
8e0180a4-bea1-4d44-923f-e3755da77bec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,3. Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
2b1cf53a-1856-4550-8d81-8ba35c6d201c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"Diabetes, obesity, and EH",False,"Diabetes, obesity, and EH",,,,
b168ae0f-d08d-4591-b2bb-e14010f8ae64,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"The linkage between diabetes and EH, and obesity and EH, appears strong and direct. Because insulin is a dietary-induced mediator of sympathetic activity, the elevated insulin levels in insulin-resistant diabetes can directly promote hypertension. Insulin can also lead to an increase in peripheral resistance via its mitogenic effect on vascular smooth muscle that causes hypertrophy in the medial vascular layers and a decrease in lumen size.",True,"Diabetes, obesity, and EH",,,,
a13d0374-85ce-425b-853d-a9c452f1c8d4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"Obesity can also induce hypertension through release of angiotensinogen from more abundant adipocytes, thus providing more substrate for the RAA system. The increase in body mass is also accompanied by an increase in blood volume, and that blood may be more viscous as the large population of adipocytes release coagulative proteins, including prothrombin.",True,"Diabetes, obesity, and EH",,,,
ae207fa7-0a3a-4718-8206-4d468cbde84d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,Secondary Hypertension,False,Secondary Hypertension,,,,
01f825d4-d617-42f9-b62c-33584ef407ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"Although not as common, there are numerous causes of secondary hypertension. There are some distinguishing features that are clinically useful to distinguish it from EH. Your first heads-up is if the patient is younger and not in the typical range for EH (> fifty years old). Secondary hypertension also tends to be more severe, and BP can rise dramatically; EH does not have a rapid onset. While EH often comes with family history, secondary hypertension is more sporadic.",True,Secondary Hypertension,,,,
ac778a74-f870-4ef5-b617-d3f3fd0ad4c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"Suspicion of secondary hypertension can usually be confirmed by urinalysis that reveals the underlying issue (see table 3.1 for some common causes and cues for diagnosis). Disturbances in electrolytes and creatinine accompany the renal and mineralocorticoid-based diseases. Pheochromocytoma is rare and accounts for 0.2 percent of secondary hypertension cases (however, it is much more common in exam questions than it is in the clinic!).",True,Secondary Hypertension,,,,
fc24c861-eadd-4fb3-934c-6bf05ae195e8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"Drugs that disrupt the angiotensinogen pathways (e.g., estrogens), are sympathomimetic (e.g., over-the-counter cold remedies), or promote sodium and water retention (e.g., NSAIDS) can all produce secondary hypertension.",True,Secondary Hypertension,,,,
c5a9d8e4-5ce9-4a1f-abf2-2c6021a7abaa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,Consequences of Hypertension,False,Consequences of Hypertension,,,,
8af59a67-2c51-440e-ab29-0507a4c24df7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"As most hypertensive patients are asymptomatic, the condition can be left unmanaged and allowed to produce significant chronic effects. Most of these effects are caused by the extra work placed on the heart with the increased afterload and the damage to the interior of the vasculature.",True,Consequences of Hypertension,,,,
2fad48e0-c192-4de6-86fd-0068b44ba4bf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"The excess afterload can lead to systolic dysfunction and eventually heart failure with reduced ejection fraction (HFREF). In response to the excessive afterload the left ventricle can hypertrophy, causing a loss of compliance diastolic dysfunction and eventually heart failure with normal ejection fraction (HFNEF). The increased workload and muscle mass also increase the myocardial oxygen demand. This increase in demand often occurs at the same time that blood supply is diminished by concurrent atherosclerosis that is accelerated by the hypertension-induced arterial damage. Consequently, with high demand and low supply, the patient is prone to ischemia and myocardial infarction.",True,Consequences of Hypertension,,,,
716c5fb7-453d-4b88-90dc-1ccc3a767e77,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"The arterial damage will also promote thrombosis and atheroemboli, so risk of embolic stroke is raised. Risk of hemorrhagic stroke is also increased as the vessel ways become weak. The large vessels are also at risk of being unable to counteract raised pressure (remember Laplace’s law?), so aortic aneurysm and dissection can also occur.",True,Consequences of Hypertension,,,,
6e39d358-58fd-40cf-a861-e261a26fc797,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"High pressures entering the renal circulation can lead to nephrosclerosis. As renal function declines, a vicious cycle forms with renal failure exacerbating hypertension that exacerbates renal failure.",True,Consequences of Hypertension,,,,
0c95f129-24a7-40eb-b34f-45ed94d12708,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,Hypertensive Crisis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
0c95f129-24a7-40eb-b34f-45ed94d12708,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,Consequences of Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
0c95f129-24a7-40eb-b34f-45ed94d12708,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,Secondary Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
0c95f129-24a7-40eb-b34f-45ed94d12708,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,Essential Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
0c95f129-24a7-40eb-b34f-45ed94d12708,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,3. Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
0f0f3f95-f02c-4202-9d44-5fcd1ebdecc9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,Hypertensive Crisis,False,Hypertensive Crisis,,,,
3de5530e-f354-4ee7-9fd3-c141ad49a833,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"Most commonly caused by a hemodynamic insult overlaid on chronic hypertension, a hypertensive crisis is a severe elevation of blood pressure that can become life threatening through raising intracranial pressure. The rise in intracranial pressure produces severe headache, blurred vision, confusion, or even coma and is referred to as hypertensive encephalopathy. Funduscopy reveals retinal hemorrhages, exudates, and sometimes papilledema. The massive afterload on the left ventricle can precipitate angina. Therapy must be rapid to prevent permanent vascular consequences, and if administered in time the acute changes are usually reversed. However, the underlying cause of the crisis (usually renal failure) will persist.",True,Hypertensive Crisis,,,,
f957bbb6-a276-40f9-b1c1-4feadab26099,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,Text,False,Text,,,,
88376452-891e-4714-b095-f910da3758dd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"Brown, Jenifer M., Gordon H. Williams, and Leonard S. Lilly. “Hypertension.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 13. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
00ee4672-024b-4f5b-ab6b-312b69ddfdaf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"Hajar, Rachel. “Framingham Contribution to Cardiovascular Disease.” Heart Views 17, no. 2 (April–June 2016): 78–81. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4966216.",True,Text,,,,
3feeea8d-02f4-429c-a96a-94d6e17b9b97,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"Iqbal, Arshad Muhammad, and Syed F. Jaml. Essential Hypertension. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK539859/, CC BY 4.0.",True,Text,,,,
1dd206c4-d065-475c-b987-ea3db614ff83,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Essential Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/#chapter-27-section-1,"Page, Michael R. “The JNC 8 Hypertension Guidelines: An In-Depth Guide.” Evidence-Based Diabetes Management 20, no. SP1  (January 2014). https://www.ajmc.com/view/the-jnc-8-hypertension-guidelines-an-in-depth-guide.",True,Text,,,,
714182b9-1678-47a9-878e-a204ebf628a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"The current guidelines (JNC 8, 2017) list the following pressures and categories to define hypertension:",True,Text,,,,
fa285ab6-8127-42ad-a509-4649921eefb0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,JNC,False,JNC,,,,
dc9880d8-a0b9-462c-8a60-2f7ce696d781,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,Hypertensive Crisis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
dc9880d8-a0b9-462c-8a60-2f7ce696d781,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,Consequences of Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
dc9880d8-a0b9-462c-8a60-2f7ce696d781,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,Secondary Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
dc9880d8-a0b9-462c-8a60-2f7ce696d781,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,Essential Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
dc9880d8-a0b9-462c-8a60-2f7ce696d781,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"Hypertension can be categorized as either essential or secondary. Secondary is much less common and a consequence of another condition (e.g., renal or endocrine disease). Essential hypertension (EH), despite being the prevalent form, is poorly understood but can be attributed to a problem with either cardiac output or peripheral resistance (i.e., the components of blood pressure regulation). Because multiple factors contribute to these components AND there is evidence of some genetic component to hypertension AND due to the contribution from environmental factors, essential hypertension can be considered a “description” rather than a “diagnosis.” Primary abnormalities that may contribute to essential hypertension are shown in figure 3.1.",True,JNC,Figure 3.1,3. Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
d412dc39-7f68-4490-a021-89c72cb7b209,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,Genetic components of essential hypertension,False,Genetic components of essential hypertension,,,,
e540fba8-0ec4-459c-8268-fd6d306fa509,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"No single loci has been identified as causing hypertension, but strong familial histories suggest polygenic causes (i.e., multiple loci are involved). Much attention has been paid to genes involved with enzymes and receptor production within the Renin-Angiotensin-Aldosterone (RAA) system because of its critical role in blood pressure control through sodium and volume regulation. Similarly genes involved with renal regulation of sodium have been studied. Our inability to demonstrate a genetic basis to hypertension is also consistent with significant environmental causes.",True,Genetic components of essential hypertension,,,,
35370b6c-17ba-4421-95aa-8aec84cc2583,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,Systemic abnormalities and EH,False,Systemic abnormalities and EH,,,,
d77f1465-0d0d-4beb-927a-ed21d7886b7b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,Hypertensive Crisis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
d77f1465-0d0d-4beb-927a-ed21d7886b7b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,Consequences of Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
d77f1465-0d0d-4beb-927a-ed21d7886b7b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,Secondary Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
d77f1465-0d0d-4beb-927a-ed21d7886b7b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,Essential Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
d77f1465-0d0d-4beb-927a-ed21d7886b7b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"Since Blood Pressure = Cardiac Output x Peripheral Resistance, it should be easy to imagine why aberrant rises in cardiac output (e.g., increased sympathetic tone) or peripheral resistance (e.g., low levels of vasodilators) would cause a rise in blood pressure (BP). Some of those aberrations of the acute BP control mechanisms are in figure 3.1, but this is clearly half the story as there are chronic control mechanisms that should surely compensation for loss of acute control. What this means is, for hypertension to be sustained, the kidney must be “in on the hypertension act.” While the kidney itself can be responsible for volume-based hypertension (dysregulated renal blood flow, ion channels defects, etc.), there are deficits in renal control in hypertension. Renin levels are normal or high in 70 to 75 percent of EH patients—and of course they should be low as elevated BP should suppress renin secretion. So while this begins a chicken-and-egg scenario, for hypertension to be sustained, both acute and chronic control mechanisms must fail.",True,Systemic abnormalities and EH,Figure 3.1,3. Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.1-scaled.jpg,Figure 3.1: Potential sources of essential hypertension.
bc34c9eb-82d7-45ac-b2da-25f2b6f28b2f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"Diabetes, obesity, and EH",False,"Diabetes, obesity, and EH",,,,
2659f0b4-3dba-4967-83c6-4e0ee2d91067,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"The linkage between diabetes and EH, and obesity and EH, appears strong and direct. Because insulin is a dietary-induced mediator of sympathetic activity, the elevated insulin levels in insulin-resistant diabetes can directly promote hypertension. Insulin can also lead to an increase in peripheral resistance via its mitogenic effect on vascular smooth muscle that causes hypertrophy in the medial vascular layers and a decrease in lumen size.",True,"Diabetes, obesity, and EH",,,,
6a4a28c0-6318-4707-8d27-608121ec97d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"Obesity can also induce hypertension through release of angiotensinogen from more abundant adipocytes, thus providing more substrate for the RAA system. The increase in body mass is also accompanied by an increase in blood volume, and that blood may be more viscous as the large population of adipocytes release coagulative proteins, including prothrombin.",True,"Diabetes, obesity, and EH",,,,
10df0535-6052-477d-9398-867631b5e17f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,Secondary Hypertension,False,Secondary Hypertension,,,,
e37b17b0-07cb-4cae-8220-92a1b6f0cf63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"Although not as common, there are numerous causes of secondary hypertension. There are some distinguishing features that are clinically useful to distinguish it from EH. Your first heads-up is if the patient is younger and not in the typical range for EH (> fifty years old). Secondary hypertension also tends to be more severe, and BP can rise dramatically; EH does not have a rapid onset. While EH often comes with family history, secondary hypertension is more sporadic.",True,Secondary Hypertension,,,,
b54424c7-a61f-4ab5-a19d-dc87ed9d1466,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"Suspicion of secondary hypertension can usually be confirmed by urinalysis that reveals the underlying issue (see table 3.1 for some common causes and cues for diagnosis). Disturbances in electrolytes and creatinine accompany the renal and mineralocorticoid-based diseases. Pheochromocytoma is rare and accounts for 0.2 percent of secondary hypertension cases (however, it is much more common in exam questions than it is in the clinic!).",True,Secondary Hypertension,,,,
12dfc725-65b8-4776-be89-65610e8ccf69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"Drugs that disrupt the angiotensinogen pathways (e.g., estrogens), are sympathomimetic (e.g., over-the-counter cold remedies), or promote sodium and water retention (e.g., NSAIDS) can all produce secondary hypertension.",True,Secondary Hypertension,,,,
2c69e7b0-3ef1-463e-b862-21b1a62539f2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,Consequences of Hypertension,False,Consequences of Hypertension,,,,
53edd94b-3dd5-4223-b764-5128ba6cfebb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"As most hypertensive patients are asymptomatic, the condition can be left unmanaged and allowed to produce significant chronic effects. Most of these effects are caused by the extra work placed on the heart with the increased afterload and the damage to the interior of the vasculature.",True,Consequences of Hypertension,,,,
5c99bcca-1c8d-42c2-a60d-2d94a46c336f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"The excess afterload can lead to systolic dysfunction and eventually heart failure with reduced ejection fraction (HFREF). In response to the excessive afterload the left ventricle can hypertrophy, causing a loss of compliance diastolic dysfunction and eventually heart failure with normal ejection fraction (HFNEF). The increased workload and muscle mass also increase the myocardial oxygen demand. This increase in demand often occurs at the same time that blood supply is diminished by concurrent atherosclerosis that is accelerated by the hypertension-induced arterial damage. Consequently, with high demand and low supply, the patient is prone to ischemia and myocardial infarction.",True,Consequences of Hypertension,,,,
2b3616b4-d971-45a7-903a-242567c6f30d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"The arterial damage will also promote thrombosis and atheroemboli, so risk of embolic stroke is raised. Risk of hemorrhagic stroke is also increased as the vessel ways become weak. The large vessels are also at risk of being unable to counteract raised pressure (remember Laplace’s law?), so aortic aneurysm and dissection can also occur.",True,Consequences of Hypertension,,,,
63ea7797-ab90-401a-b128-fd35284d18bb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"High pressures entering the renal circulation can lead to nephrosclerosis. As renal function declines, a vicious cycle forms with renal failure exacerbating hypertension that exacerbates renal failure.",True,Consequences of Hypertension,,,,
03ca9c97-556f-4cff-8943-61cdbe56b7ed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,Hypertensive Crisis,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
03ca9c97-556f-4cff-8943-61cdbe56b7ed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,Consequences of Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
03ca9c97-556f-4cff-8943-61cdbe56b7ed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,Secondary Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
03ca9c97-556f-4cff-8943-61cdbe56b7ed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,Essential Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
03ca9c97-556f-4cff-8943-61cdbe56b7ed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"The retinal circulation provides a direct window into the state of the vasculature. Rapid onset and severe hypertension may burst small retinal vessels and produce local infarctions. In more chronic cases, arterial narrowing and medial hypertrophy of the retinal vessel can be seen. As the chronic hypertension worsens, arterial sclerosis is evident. While these chronic effects may not produce functional issues, they are at least an accessible indicator of the vascular status. The consequences of hypertension are summarized in figure 3.2.",True,Consequences of Hypertension,Figure 3.2,3. Hypertension,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/3.3-newest-scaled.jpg,Figure 3.2: Consequences of hypertension.
d6085829-83b6-496d-a1a0-5c7c1e914bf3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,Hypertensive Crisis,False,Hypertensive Crisis,,,,
bd6b7d24-c279-416a-932b-890b7cb82abd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"Most commonly caused by a hemodynamic insult overlaid on chronic hypertension, a hypertensive crisis is a severe elevation of blood pressure that can become life threatening through raising intracranial pressure. The rise in intracranial pressure produces severe headache, blurred vision, confusion, or even coma and is referred to as hypertensive encephalopathy. Funduscopy reveals retinal hemorrhages, exudates, and sometimes papilledema. The massive afterload on the left ventricle can precipitate angina. Therapy must be rapid to prevent permanent vascular consequences, and if administered in time the acute changes are usually reversed. However, the underlying cause of the crisis (usually renal failure) will persist.",True,Hypertensive Crisis,,,,
29f381ab-6741-4734-acf9-ed953436ecbf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,Text,False,Text,,,,
80012500-e300-4d3f-8ce4-c66693a6d7ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"Brown, Jenifer M., Gordon H. Williams, and Leonard S. Lilly. “Hypertension.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 13. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
b40d31fb-d365-4afe-8e2e-8e9fa450070a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"Hajar, Rachel. “Framingham Contribution to Cardiovascular Disease.” Heart Views 17, no. 2 (April–June 2016): 78–81. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4966216.",True,Text,,,,
438ac41c-131c-4fcf-986d-4ac3df8ff2f2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"Iqbal, Arshad Muhammad, and Syed F. Jaml. Essential Hypertension. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK539859/, CC BY 4.0.",True,Text,,,,
60b76b63-0615-4f64-bbe3-ee50d47ad4aa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,3. Hypertension,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-3-hypertension/,"Page, Michael R. “The JNC 8 Hypertension Guidelines: An In-Depth Guide.” Evidence-Based Diabetes Management 20, no. SP1  (January 2014). https://www.ajmc.com/view/the-jnc-8-hypertension-guidelines-an-in-depth-guide.",True,Text,,,,
542c40cb-0157-4bdb-8e18-253f38324396,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"For whichever reason the end effect of the failure is a decline in blood flow out of the heart, and consequently congestion on the way in.",True,Text,,,,
7793dbfa-5e5b-4555-9631-e10c6b1d4a99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,Table 2.1: Changes in cardiac function in different disease states.,True,Text,,,,
810dee93-c004-4109-b99d-0c58c90f8bc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
810dee93-c004-4109-b99d-0c58c90f8bc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
810dee93-c004-4109-b99d-0c58c90f8bc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
810dee93-c004-4109-b99d-0c58c90f8bc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
810dee93-c004-4109-b99d-0c58c90f8bc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
9d443965-9456-4656-a0f9-1e1e37fce404,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"In reality there is a great deal of overlap between these forms of heart failure, and elements of both can be present in the same patient. Similarly, as both forms result in congestion before the heart and reduced flow after it, they are hard to immediately distinguish. Consequently the type and degree of failure is now categorized by the effect on ejection fraction that can help distinguish the source of the problem.",True,Text,,,,
33c5d98f-6bcc-40b2-9a97-f4a5cf465f1c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
33c5d98f-6bcc-40b2-9a97-f4a5cf465f1c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
33c5d98f-6bcc-40b2-9a97-f4a5cf465f1c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
33c5d98f-6bcc-40b2-9a97-f4a5cf465f1c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
33c5d98f-6bcc-40b2-9a97-f4a5cf465f1c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
20622c34-1a4f-473e-973b-176ee18cd7b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,Ejection Fraction in Systolic Failure,False,Ejection Fraction in Systolic Failure,,,,
8313e09f-8062-4d5c-992f-418a2f86e873,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Let us first relate this to systolic failure by looking at what happens when the contractility of the myocardium is reduced. In systolic failure, there is a problem getting blood out of the heart, so the volume of blood coming out of the heart per beat (EDV-ESV) is reduced. However, the end diastolic volume will remain the same, or more likely rise. So our ejection fraction is reduced. Consequently, if you have a reduced ejection fraction you know you have a systolic failure. So to improve diagnosis, systolic failure is now referred to as heart failure with a reduced ejection fraction (HFREF).",True,Ejection Fraction in Systolic Failure,,,,
bb4d5498-c998-405e-bfe2-bdc0fdb98ee3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
bb4d5498-c998-405e-bfe2-bdc0fdb98ee3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
bb4d5498-c998-405e-bfe2-bdc0fdb98ee3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
bb4d5498-c998-405e-bfe2-bdc0fdb98ee3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
bb4d5498-c998-405e-bfe2-bdc0fdb98ee3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
a6ecac52-4f7f-4f9a-959c-73163b2c45e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"So systolic failure is referred to as HFREF, but what started as a problem emptying the heart has led to congestion and has produced a problem getting blood into the heart. Let us compare this with diastolic failure.",True,Ejection Fraction in Systolic Failure,,,,
94108388-5e0d-4c37-bf0b-ca7771e3c675,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,Ejection Fraction in Diastolic Failure,False,Ejection Fraction in Diastolic Failure,,,,
4a4369ee-b8dd-4481-b713-a6c69f9c6ce7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Remember that in diastolic failure there is a problem relaxing/filling the ventricle. Consequently EDV tends to be lower than normal, and this lower volume of blood in the chamber is relatively easy for the heart to expel. So proportionately, the ejection fraction can be maintained, even if the absolute stroke volume may be low. This is now classified as heart failure with a normal ejection fraction (HFNEF).",True,Ejection Fraction in Diastolic Failure,,,,
3c7cd1cb-4846-4b2e-a25f-4cab6021fbc9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"The pathophysiological consequences of HFNEF stem from the poor relaxation of the ventricle and/or ability to accept blood. When the ventricle is noncompliant during diastole (i.e., does not relax properly), it does not take much blood volume to enter the chamber before the ventricle pressure begins to rise. This rise in ventricular pressure opposes the entry of more blood, so it accumulates in the atrium. Atrial pressure rises and venous return is impeded, so blood becomes congested in the venous system.",True,Ejection Fraction in Diastolic Failure,,,,
41492948-d42e-48d2-8d92-5f2fa12f7f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
41492948-d42e-48d2-8d92-5f2fa12f7f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
41492948-d42e-48d2-8d92-5f2fa12f7f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
41492948-d42e-48d2-8d92-5f2fa12f7f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
41492948-d42e-48d2-8d92-5f2fa12f7f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
7c1b6d8d-ee1a-4cfe-be3e-3be6c7664e69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,True,Ejection Fraction in Diastolic Failure,,,,
e63043fd-51c9-4f41-a0c6-e96a7748fc36,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Initial responses to the diminished cardiac output include the acute compensatory responses to low blood pressure, myocardial stretch, or changes in renal perfusion. Let us do a quick review.",True,Ejection Fraction in Diastolic Failure,,,,
2457bc27-6e6b-4146-8364-866cf6245fb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"The reduced cardiac output leads to a reduced arterial blood pressure, which, in combination with low volume exiting the heart, results in lower blood flow. With less blood exiting the heart, more remains in the chamber, particularly with systolic failure, so the myocardium is stretched. These three factors (pressure, flow, and myocardial stretch) elicit mechanical, neural, and hormone responses intended to correct the fall in pressure, resume flow, and clear the heart of congestion—but these responses are intended for a normal heart, not one undergoing failure.",True,Ejection Fraction in Diastolic Failure,,,,
827a6f0f-2995-441d-a84f-1326feff6ad8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
827a6f0f-2995-441d-a84f-1326feff6ad8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
827a6f0f-2995-441d-a84f-1326feff6ad8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
827a6f0f-2995-441d-a84f-1326feff6ad8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
827a6f0f-2995-441d-a84f-1326feff6ad8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
f4564ed9-680a-4eb9-98a0-9300621443d8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"These compensatory effects are all attempts to improve cardiac output and blood pressure, but the failing heart is being forced to work harder against an increased afterload and move more volume. Consequently, but for the natriuretic peptides, these responses are maladaptive in the long term, and chronic changes to the heart are instigated.",True,Ejection Fraction in Diastolic Failure,,,,
e31b68ab-dffc-4c91-8adf-bc3c6dfa5449,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,Chronic Remodeling and Hypertrophy,False,Chronic Remodeling and Hypertrophy,,,,
38a6b3ec-f8b6-41bd-a4dc-855ba9398345,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"The long-term structural changes begin with additional wall stress in the failing heart interacting with neurohormonal and cytokine alterations, but the wall stress seems to be an important instigator of hypertrophy and remodeling. Stress can be placed on the chamber walls in two major ways.",True,Chronic Remodeling and Hypertrophy,,,,
3d505d61-d695-4456-81c2-16b0858e0ef1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
3d505d61-d695-4456-81c2-16b0858e0ef1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
3d505d61-d695-4456-81c2-16b0858e0ef1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
3d505d61-d695-4456-81c2-16b0858e0ef1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
3d505d61-d695-4456-81c2-16b0858e0ef1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
cf5247ca-13e8-49ce-a929-e13d964bdeee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
cf5247ca-13e8-49ce-a929-e13d964bdeee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
cf5247ca-13e8-49ce-a929-e13d964bdeee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
cf5247ca-13e8-49ce-a929-e13d964bdeee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
cf5247ca-13e8-49ce-a929-e13d964bdeee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
af81a211-a1f5-4981-aeb8-b5e176b28af0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
af81a211-a1f5-4981-aeb8-b5e176b28af0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
af81a211-a1f5-4981-aeb8-b5e176b28af0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
af81a211-a1f5-4981-aeb8-b5e176b28af0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
af81a211-a1f5-4981-aeb8-b5e176b28af0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
1688bd5c-bfae-42ba-abd9-825ce316194a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Myocytes may also be lost through either apoptosis or necrosis. As hypertrophy occurs the blood supply to the thickening wall becomes inadequate so infarction and consequent necrosis are more likely. Factors that promote myocyte apoptosis are all present during heart failure and include elevated catecholamines, Angiotensin II, inflammatory cytokines, and wall stress.",True,Chronic Remodeling and Hypertrophy,,,,
bb79e7cd-ae7b-4e7e-9b25-d6a2a2fa57c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"These same factors also disrupt gene expression in myocytes and cause intracellular deficits, including loss of Ca++ homeostasis and production of high-energy phosphates. While the mechanisms of these intracellular effects is still being heavily researched, the inability to control calcium or regulate high-energy phosphates obviously has implications of excitation–contraction coupling.",True,Chronic Remodeling and Hypertrophy,,,,
384bc000-79c1-4a05-be16-e91fa7cc8b07,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"So while hypertrophy may seem a sensible response in the failing heart, the patterns and inflammation and stress-driven changes are eventually maladaptive and lead to a progressive decline in cardiac function.",True,Chronic Remodeling and Hypertrophy,,,,
b96a14b3-90c1-46d9-85a7-3d8097f1cc0b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,Clinical Manifestations of Heart Failure,False,Clinical Manifestations of Heart Failure,,,,
8eedeb9c-8875-4207-8dc0-63d9714411a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
8eedeb9c-8875-4207-8dc0-63d9714411a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
8eedeb9c-8875-4207-8dc0-63d9714411a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
8eedeb9c-8875-4207-8dc0-63d9714411a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
8eedeb9c-8875-4207-8dc0-63d9714411a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
cd53d0f7-ff4a-4644-bb06-f1b12dd8d8d7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"If the right heart fails, there is a rise in systemic venous pressure and peripheral edema arises. There may be abdominal discomfort as the liver becomes engorged and a loss of appetite or nausea as gastrointestinal edema arises. If the left heart fails, then the pulmonary circulation is exposed to the congestion and pulmonary edema arises.",True,Clinical Manifestations of Heart Failure,,,,
f01b9785-90a8-4f1f-9af6-b2abdb605faa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Low cardiac output reduces renal filtration, so urine formation maybe impaired. Similarly cerebral blood flow may be compromised, causing dulled mental status.",True,Clinical Manifestations of Heart Failure,,,,
aae92405-fd79-4bad-b17c-3704ca13b242,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Orthopnea arises when the patient lays down and venous return toward the failing left ventricle increases, compounding the pulmonary congestion. Patients often sleep propped up on pillows to elevate the heart and lungs. In severe cases the patient may only be able to sleep upright in a chair.",True,Clinical Manifestations of Heart Failure,,,,
d45321c9-d9df-49c7-a18d-3cd9efdf64e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,Text,False,Text,,,,
0dade292-7120-4fea-a845-e26eeb3159a3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Eberly, Lauren A., Eldrin F. Lewis, and Leonard S. Lilly. “Heart Failure.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e, edited by Leonard S. Lilly, Chapter 9. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
d3239a6f-3c3d-4562-9ca8-835f21d500e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-4,"Malik, Ahmad, Daniel Brito, Sarosh Vaqar, and Lovely Chhabra. Congestive Heart Failure. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430873/, CC BY 4.0.",True,Text,,,,
bceb2425-382b-4be9-b89a-850f5b5bf48e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"For whichever reason the end effect of the failure is a decline in blood flow out of the heart, and consequently congestion on the way in.",True,Text,,,,
0d66cb6c-1e2f-414f-a689-65e044dc8a8c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,Table 2.1: Changes in cardiac function in different disease states.,True,Text,,,,
f961d398-93af-4272-9222-050f0b5ad8d7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
f961d398-93af-4272-9222-050f0b5ad8d7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
f961d398-93af-4272-9222-050f0b5ad8d7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
f961d398-93af-4272-9222-050f0b5ad8d7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
f961d398-93af-4272-9222-050f0b5ad8d7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
b40b36d7-3146-43c9-80b1-2cb609a8cfc5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"In reality there is a great deal of overlap between these forms of heart failure, and elements of both can be present in the same patient. Similarly, as both forms result in congestion before the heart and reduced flow after it, they are hard to immediately distinguish. Consequently the type and degree of failure is now categorized by the effect on ejection fraction that can help distinguish the source of the problem.",True,Text,,,,
a1494fe6-e962-40d4-acdd-7c11e88f456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
a1494fe6-e962-40d4-acdd-7c11e88f456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
a1494fe6-e962-40d4-acdd-7c11e88f456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
a1494fe6-e962-40d4-acdd-7c11e88f456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
a1494fe6-e962-40d4-acdd-7c11e88f456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
52218489-caa7-40b4-97e7-955d65c12c09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,Ejection Fraction in Systolic Failure,False,Ejection Fraction in Systolic Failure,,,,
c1cb9de0-cb54-4c4e-bc31-d524e9c76a13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Let us first relate this to systolic failure by looking at what happens when the contractility of the myocardium is reduced. In systolic failure, there is a problem getting blood out of the heart, so the volume of blood coming out of the heart per beat (EDV-ESV) is reduced. However, the end diastolic volume will remain the same, or more likely rise. So our ejection fraction is reduced. Consequently, if you have a reduced ejection fraction you know you have a systolic failure. So to improve diagnosis, systolic failure is now referred to as heart failure with a reduced ejection fraction (HFREF).",True,Ejection Fraction in Systolic Failure,,,,
4aa624da-db54-4d04-a86d-516d95ac0a98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
4aa624da-db54-4d04-a86d-516d95ac0a98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
4aa624da-db54-4d04-a86d-516d95ac0a98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
4aa624da-db54-4d04-a86d-516d95ac0a98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
4aa624da-db54-4d04-a86d-516d95ac0a98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
e9a4fa90-6383-4b27-9882-0c0f2e305231,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"So systolic failure is referred to as HFREF, but what started as a problem emptying the heart has led to congestion and has produced a problem getting blood into the heart. Let us compare this with diastolic failure.",True,Ejection Fraction in Systolic Failure,,,,
94025e06-48c2-4bae-84c2-b2b486db5c50,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,Ejection Fraction in Diastolic Failure,False,Ejection Fraction in Diastolic Failure,,,,
92af5a01-2852-485e-b3da-147d8831caa8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Remember that in diastolic failure there is a problem relaxing/filling the ventricle. Consequently EDV tends to be lower than normal, and this lower volume of blood in the chamber is relatively easy for the heart to expel. So proportionately, the ejection fraction can be maintained, even if the absolute stroke volume may be low. This is now classified as heart failure with a normal ejection fraction (HFNEF).",True,Ejection Fraction in Diastolic Failure,,,,
776cef7b-7578-49ea-a282-f93cb05a65b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"The pathophysiological consequences of HFNEF stem from the poor relaxation of the ventricle and/or ability to accept blood. When the ventricle is noncompliant during diastole (i.e., does not relax properly), it does not take much blood volume to enter the chamber before the ventricle pressure begins to rise. This rise in ventricular pressure opposes the entry of more blood, so it accumulates in the atrium. Atrial pressure rises and venous return is impeded, so blood becomes congested in the venous system.",True,Ejection Fraction in Diastolic Failure,,,,
ea9e90ae-3d42-4154-9a61-25ccd1ccc18a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
ea9e90ae-3d42-4154-9a61-25ccd1ccc18a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
ea9e90ae-3d42-4154-9a61-25ccd1ccc18a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
ea9e90ae-3d42-4154-9a61-25ccd1ccc18a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
ea9e90ae-3d42-4154-9a61-25ccd1ccc18a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
3e1e98c0-1584-4be5-a5c3-fa4838e45b06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,True,Ejection Fraction in Diastolic Failure,,,,
00b29cb3-c950-4c57-99ad-6b48667d491e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Initial responses to the diminished cardiac output include the acute compensatory responses to low blood pressure, myocardial stretch, or changes in renal perfusion. Let us do a quick review.",True,Ejection Fraction in Diastolic Failure,,,,
ee6fe54c-56c1-45eb-99e7-da553fe153ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"The reduced cardiac output leads to a reduced arterial blood pressure, which, in combination with low volume exiting the heart, results in lower blood flow. With less blood exiting the heart, more remains in the chamber, particularly with systolic failure, so the myocardium is stretched. These three factors (pressure, flow, and myocardial stretch) elicit mechanical, neural, and hormone responses intended to correct the fall in pressure, resume flow, and clear the heart of congestion—but these responses are intended for a normal heart, not one undergoing failure.",True,Ejection Fraction in Diastolic Failure,,,,
317ebf37-4eb9-40b2-b08b-4171810461a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
317ebf37-4eb9-40b2-b08b-4171810461a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
317ebf37-4eb9-40b2-b08b-4171810461a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
317ebf37-4eb9-40b2-b08b-4171810461a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
317ebf37-4eb9-40b2-b08b-4171810461a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
035399bb-a21f-45ae-bdc8-83f0ed8a59c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"These compensatory effects are all attempts to improve cardiac output and blood pressure, but the failing heart is being forced to work harder against an increased afterload and move more volume. Consequently, but for the natriuretic peptides, these responses are maladaptive in the long term, and chronic changes to the heart are instigated.",True,Ejection Fraction in Diastolic Failure,,,,
17b36619-38a8-403f-8a63-8dee5de36c8b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,Chronic Remodeling and Hypertrophy,False,Chronic Remodeling and Hypertrophy,,,,
1de4a5eb-6899-4ef4-a7b0-88922ecc5af2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"The long-term structural changes begin with additional wall stress in the failing heart interacting with neurohormonal and cytokine alterations, but the wall stress seems to be an important instigator of hypertrophy and remodeling. Stress can be placed on the chamber walls in two major ways.",True,Chronic Remodeling and Hypertrophy,,,,
5067ad0e-7bb0-44d4-8216-44522f224a85,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
5067ad0e-7bb0-44d4-8216-44522f224a85,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
5067ad0e-7bb0-44d4-8216-44522f224a85,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
5067ad0e-7bb0-44d4-8216-44522f224a85,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
5067ad0e-7bb0-44d4-8216-44522f224a85,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
58c2c335-51e9-4a72-a4d3-7e4268fc8d4a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
58c2c335-51e9-4a72-a4d3-7e4268fc8d4a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
58c2c335-51e9-4a72-a4d3-7e4268fc8d4a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
58c2c335-51e9-4a72-a4d3-7e4268fc8d4a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
58c2c335-51e9-4a72-a4d3-7e4268fc8d4a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
38dd1487-acaf-4119-a3fe-2b19bd2307ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
38dd1487-acaf-4119-a3fe-2b19bd2307ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
38dd1487-acaf-4119-a3fe-2b19bd2307ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
38dd1487-acaf-4119-a3fe-2b19bd2307ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
38dd1487-acaf-4119-a3fe-2b19bd2307ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
6d2179bc-85d0-4d63-8e92-2f15f21295cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Myocytes may also be lost through either apoptosis or necrosis. As hypertrophy occurs the blood supply to the thickening wall becomes inadequate so infarction and consequent necrosis are more likely. Factors that promote myocyte apoptosis are all present during heart failure and include elevated catecholamines, Angiotensin II, inflammatory cytokines, and wall stress.",True,Chronic Remodeling and Hypertrophy,,,,
5400d348-5cbe-4059-8458-9f745c15f8b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"These same factors also disrupt gene expression in myocytes and cause intracellular deficits, including loss of Ca++ homeostasis and production of high-energy phosphates. While the mechanisms of these intracellular effects is still being heavily researched, the inability to control calcium or regulate high-energy phosphates obviously has implications of excitation–contraction coupling.",True,Chronic Remodeling and Hypertrophy,,,,
d6967077-9d3f-49af-8509-e99bd23b1712,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"So while hypertrophy may seem a sensible response in the failing heart, the patterns and inflammation and stress-driven changes are eventually maladaptive and lead to a progressive decline in cardiac function.",True,Chronic Remodeling and Hypertrophy,,,,
ec98e246-d0f9-4e3d-b5ab-95fafd86a086,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,Clinical Manifestations of Heart Failure,False,Clinical Manifestations of Heart Failure,,,,
8f1fa5f5-da7d-43b8-8af7-c18ec664f8bf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
8f1fa5f5-da7d-43b8-8af7-c18ec664f8bf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
8f1fa5f5-da7d-43b8-8af7-c18ec664f8bf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
8f1fa5f5-da7d-43b8-8af7-c18ec664f8bf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
8f1fa5f5-da7d-43b8-8af7-c18ec664f8bf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
eb7b6109-0ad8-49fc-a55c-2e37d0de64fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"If the right heart fails, there is a rise in systemic venous pressure and peripheral edema arises. There may be abdominal discomfort as the liver becomes engorged and a loss of appetite or nausea as gastrointestinal edema arises. If the left heart fails, then the pulmonary circulation is exposed to the congestion and pulmonary edema arises.",True,Clinical Manifestations of Heart Failure,,,,
8abee636-284c-40b0-a8ab-0b62256548da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Low cardiac output reduces renal filtration, so urine formation maybe impaired. Similarly cerebral blood flow may be compromised, causing dulled mental status.",True,Clinical Manifestations of Heart Failure,,,,
c347b9f9-43be-4d6d-8d0e-21437e201ad6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Orthopnea arises when the patient lays down and venous return toward the failing left ventricle increases, compounding the pulmonary congestion. Patients often sleep propped up on pillows to elevate the heart and lungs. In severe cases the patient may only be able to sleep upright in a chair.",True,Clinical Manifestations of Heart Failure,,,,
49f653ac-9600-43f4-b835-26ba8c69f06d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,Text,False,Text,,,,
e3070f9f-134f-4749-8e57-a74e51b2be8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Eberly, Lauren A., Eldrin F. Lewis, and Leonard S. Lilly. “Heart Failure.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e, edited by Leonard S. Lilly, Chapter 9. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
187a8888-5ede-4557-8277-3d7ba18260b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-3,"Malik, Ahmad, Daniel Brito, Sarosh Vaqar, and Lovely Chhabra. Congestive Heart Failure. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430873/, CC BY 4.0.",True,Text,,,,
b448ef46-269e-4721-a7c1-a84a5b1ed9fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"For whichever reason the end effect of the failure is a decline in blood flow out of the heart, and consequently congestion on the way in.",True,Text,,,,
8ed7fc51-f36c-4416-a830-23120e34543a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,Table 2.1: Changes in cardiac function in different disease states.,True,Text,,,,
9002d840-4ad5-47ef-ad35-5ca8e651868f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
9002d840-4ad5-47ef-ad35-5ca8e651868f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
9002d840-4ad5-47ef-ad35-5ca8e651868f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
9002d840-4ad5-47ef-ad35-5ca8e651868f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
9002d840-4ad5-47ef-ad35-5ca8e651868f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
5fb909f3-0fd4-4b94-8e63-51542e7da3a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"In reality there is a great deal of overlap between these forms of heart failure, and elements of both can be present in the same patient. Similarly, as both forms result in congestion before the heart and reduced flow after it, they are hard to immediately distinguish. Consequently the type and degree of failure is now categorized by the effect on ejection fraction that can help distinguish the source of the problem.",True,Text,,,,
e332b9fa-c987-4313-b063-0834e40643b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
e332b9fa-c987-4313-b063-0834e40643b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
e332b9fa-c987-4313-b063-0834e40643b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
e332b9fa-c987-4313-b063-0834e40643b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
e332b9fa-c987-4313-b063-0834e40643b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
f3b12887-109e-409e-bb0f-c9dd005a2805,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,Ejection Fraction in Systolic Failure,False,Ejection Fraction in Systolic Failure,,,,
750f0e07-7a4a-40ec-9603-03303fe22de0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Let us first relate this to systolic failure by looking at what happens when the contractility of the myocardium is reduced. In systolic failure, there is a problem getting blood out of the heart, so the volume of blood coming out of the heart per beat (EDV-ESV) is reduced. However, the end diastolic volume will remain the same, or more likely rise. So our ejection fraction is reduced. Consequently, if you have a reduced ejection fraction you know you have a systolic failure. So to improve diagnosis, systolic failure is now referred to as heart failure with a reduced ejection fraction (HFREF).",True,Ejection Fraction in Systolic Failure,,,,
d333b13d-2236-4298-8a83-600529dab141,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
d333b13d-2236-4298-8a83-600529dab141,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
d333b13d-2236-4298-8a83-600529dab141,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
d333b13d-2236-4298-8a83-600529dab141,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
d333b13d-2236-4298-8a83-600529dab141,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
d1ceb682-e9b0-47cc-897f-4c8cd13e9a78,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"So systolic failure is referred to as HFREF, but what started as a problem emptying the heart has led to congestion and has produced a problem getting blood into the heart. Let us compare this with diastolic failure.",True,Ejection Fraction in Systolic Failure,,,,
8051e12e-305d-4b79-aafc-48088a7c8907,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,Ejection Fraction in Diastolic Failure,False,Ejection Fraction in Diastolic Failure,,,,
7ede139c-0047-4b01-bd93-d84f34494795,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Remember that in diastolic failure there is a problem relaxing/filling the ventricle. Consequently EDV tends to be lower than normal, and this lower volume of blood in the chamber is relatively easy for the heart to expel. So proportionately, the ejection fraction can be maintained, even if the absolute stroke volume may be low. This is now classified as heart failure with a normal ejection fraction (HFNEF).",True,Ejection Fraction in Diastolic Failure,,,,
b6301847-8cec-4140-a5e4-03ef12ed5256,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"The pathophysiological consequences of HFNEF stem from the poor relaxation of the ventricle and/or ability to accept blood. When the ventricle is noncompliant during diastole (i.e., does not relax properly), it does not take much blood volume to enter the chamber before the ventricle pressure begins to rise. This rise in ventricular pressure opposes the entry of more blood, so it accumulates in the atrium. Atrial pressure rises and venous return is impeded, so blood becomes congested in the venous system.",True,Ejection Fraction in Diastolic Failure,,,,
9c99bff2-3527-4550-bc17-aa19eb5071da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
9c99bff2-3527-4550-bc17-aa19eb5071da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
9c99bff2-3527-4550-bc17-aa19eb5071da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
9c99bff2-3527-4550-bc17-aa19eb5071da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
9c99bff2-3527-4550-bc17-aa19eb5071da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
12126584-0aff-4962-8c58-3f43363cb538,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,True,Ejection Fraction in Diastolic Failure,,,,
7ee725ad-42aa-4f14-b8a1-86b07d43e8c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Initial responses to the diminished cardiac output include the acute compensatory responses to low blood pressure, myocardial stretch, or changes in renal perfusion. Let us do a quick review.",True,Ejection Fraction in Diastolic Failure,,,,
fb09930a-2e30-4d32-9bf8-21b4083c2873,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"The reduced cardiac output leads to a reduced arterial blood pressure, which, in combination with low volume exiting the heart, results in lower blood flow. With less blood exiting the heart, more remains in the chamber, particularly with systolic failure, so the myocardium is stretched. These three factors (pressure, flow, and myocardial stretch) elicit mechanical, neural, and hormone responses intended to correct the fall in pressure, resume flow, and clear the heart of congestion—but these responses are intended for a normal heart, not one undergoing failure.",True,Ejection Fraction in Diastolic Failure,,,,
cb135132-6ddb-467a-8f96-49b3b5afefb0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
cb135132-6ddb-467a-8f96-49b3b5afefb0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
cb135132-6ddb-467a-8f96-49b3b5afefb0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
cb135132-6ddb-467a-8f96-49b3b5afefb0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
cb135132-6ddb-467a-8f96-49b3b5afefb0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
314e04b4-8f40-4fc4-9880-ed891c03f483,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"These compensatory effects are all attempts to improve cardiac output and blood pressure, but the failing heart is being forced to work harder against an increased afterload and move more volume. Consequently, but for the natriuretic peptides, these responses are maladaptive in the long term, and chronic changes to the heart are instigated.",True,Ejection Fraction in Diastolic Failure,,,,
344e6656-1bc4-4154-85e4-0be10dbe6da5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,Chronic Remodeling and Hypertrophy,False,Chronic Remodeling and Hypertrophy,,,,
aa6c6f89-fa8b-42ea-8b16-570049d7cf40,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"The long-term structural changes begin with additional wall stress in the failing heart interacting with neurohormonal and cytokine alterations, but the wall stress seems to be an important instigator of hypertrophy and remodeling. Stress can be placed on the chamber walls in two major ways.",True,Chronic Remodeling and Hypertrophy,,,,
65750b87-52e5-4501-a7c4-b9b4178bf85d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
65750b87-52e5-4501-a7c4-b9b4178bf85d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
65750b87-52e5-4501-a7c4-b9b4178bf85d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
65750b87-52e5-4501-a7c4-b9b4178bf85d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
65750b87-52e5-4501-a7c4-b9b4178bf85d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
02a7d79e-1a3f-4290-b9e5-7bbe6b83c0af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
02a7d79e-1a3f-4290-b9e5-7bbe6b83c0af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
02a7d79e-1a3f-4290-b9e5-7bbe6b83c0af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
02a7d79e-1a3f-4290-b9e5-7bbe6b83c0af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
02a7d79e-1a3f-4290-b9e5-7bbe6b83c0af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
ceae2da8-d094-430f-8d92-f806f091afe0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
ceae2da8-d094-430f-8d92-f806f091afe0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
ceae2da8-d094-430f-8d92-f806f091afe0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
ceae2da8-d094-430f-8d92-f806f091afe0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
ceae2da8-d094-430f-8d92-f806f091afe0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
bc83da3d-26e0-417a-8a93-f45fc7f52abb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Myocytes may also be lost through either apoptosis or necrosis. As hypertrophy occurs the blood supply to the thickening wall becomes inadequate so infarction and consequent necrosis are more likely. Factors that promote myocyte apoptosis are all present during heart failure and include elevated catecholamines, Angiotensin II, inflammatory cytokines, and wall stress.",True,Chronic Remodeling and Hypertrophy,,,,
339dde6e-9dcb-4e6f-8c12-208e92fcce9f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"These same factors also disrupt gene expression in myocytes and cause intracellular deficits, including loss of Ca++ homeostasis and production of high-energy phosphates. While the mechanisms of these intracellular effects is still being heavily researched, the inability to control calcium or regulate high-energy phosphates obviously has implications of excitation–contraction coupling.",True,Chronic Remodeling and Hypertrophy,,,,
f7688d5b-0301-4192-a606-a9524dad29c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"So while hypertrophy may seem a sensible response in the failing heart, the patterns and inflammation and stress-driven changes are eventually maladaptive and lead to a progressive decline in cardiac function.",True,Chronic Remodeling and Hypertrophy,,,,
0283ca31-25e9-4e60-88f6-683e09486756,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,Clinical Manifestations of Heart Failure,False,Clinical Manifestations of Heart Failure,,,,
625d42f8-c714-4330-9028-4914a108f122,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
625d42f8-c714-4330-9028-4914a108f122,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
625d42f8-c714-4330-9028-4914a108f122,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
625d42f8-c714-4330-9028-4914a108f122,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
625d42f8-c714-4330-9028-4914a108f122,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
fc707a95-44a7-4324-9342-5e4dc16d9f7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"If the right heart fails, there is a rise in systemic venous pressure and peripheral edema arises. There may be abdominal discomfort as the liver becomes engorged and a loss of appetite or nausea as gastrointestinal edema arises. If the left heart fails, then the pulmonary circulation is exposed to the congestion and pulmonary edema arises.",True,Clinical Manifestations of Heart Failure,,,,
b8f7910a-7e0c-40f3-9628-76ebc693e039,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Low cardiac output reduces renal filtration, so urine formation maybe impaired. Similarly cerebral blood flow may be compromised, causing dulled mental status.",True,Clinical Manifestations of Heart Failure,,,,
c120e373-367b-4f84-9871-b0510bcc0b52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Orthopnea arises when the patient lays down and venous return toward the failing left ventricle increases, compounding the pulmonary congestion. Patients often sleep propped up on pillows to elevate the heart and lungs. In severe cases the patient may only be able to sleep upright in a chair.",True,Clinical Manifestations of Heart Failure,,,,
0a1dff3b-3985-4158-ac3c-998bccb6e99b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,Text,False,Text,,,,
776013c3-a56e-4a15-a344-88cec2366e8d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Eberly, Lauren A., Eldrin F. Lewis, and Leonard S. Lilly. “Heart Failure.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e, edited by Leonard S. Lilly, Chapter 9. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
43529936-3ebf-4c12-b994-a055f51b3bf7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-2,"Malik, Ahmad, Daniel Brito, Sarosh Vaqar, and Lovely Chhabra. Congestive Heart Failure. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430873/, CC BY 4.0.",True,Text,,,,
45c4efc7-3583-4187-87dc-f612ebdd7029,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"For whichever reason the end effect of the failure is a decline in blood flow out of the heart, and consequently congestion on the way in.",True,Text,,,,
0422d40f-c663-4bd6-8e0b-5f940a7ae018,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,Table 2.1: Changes in cardiac function in different disease states.,True,Text,,,,
e68eccaa-191b-4775-9f34-31dff7d590f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
e68eccaa-191b-4775-9f34-31dff7d590f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
e68eccaa-191b-4775-9f34-31dff7d590f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
e68eccaa-191b-4775-9f34-31dff7d590f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
e68eccaa-191b-4775-9f34-31dff7d590f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
ffe6d84c-0ca3-47d4-9b6f-4d8c738c7715,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"In reality there is a great deal of overlap between these forms of heart failure, and elements of both can be present in the same patient. Similarly, as both forms result in congestion before the heart and reduced flow after it, they are hard to immediately distinguish. Consequently the type and degree of failure is now categorized by the effect on ejection fraction that can help distinguish the source of the problem.",True,Text,,,,
fac2ad14-4257-441c-8cc8-f4219fdfa2e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
fac2ad14-4257-441c-8cc8-f4219fdfa2e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
fac2ad14-4257-441c-8cc8-f4219fdfa2e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
fac2ad14-4257-441c-8cc8-f4219fdfa2e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
fac2ad14-4257-441c-8cc8-f4219fdfa2e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
af94b715-e258-4803-921c-b19a2c139f00,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,Ejection Fraction in Systolic Failure,False,Ejection Fraction in Systolic Failure,,,,
7d7dd2e4-d0b1-4b9d-935f-314a80ed328e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Let us first relate this to systolic failure by looking at what happens when the contractility of the myocardium is reduced. In systolic failure, there is a problem getting blood out of the heart, so the volume of blood coming out of the heart per beat (EDV-ESV) is reduced. However, the end diastolic volume will remain the same, or more likely rise. So our ejection fraction is reduced. Consequently, if you have a reduced ejection fraction you know you have a systolic failure. So to improve diagnosis, systolic failure is now referred to as heart failure with a reduced ejection fraction (HFREF).",True,Ejection Fraction in Systolic Failure,,,,
7abd52cd-edd2-4483-a2a6-0720552b1fcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
7abd52cd-edd2-4483-a2a6-0720552b1fcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
7abd52cd-edd2-4483-a2a6-0720552b1fcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
7abd52cd-edd2-4483-a2a6-0720552b1fcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
7abd52cd-edd2-4483-a2a6-0720552b1fcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
0635ea22-13b1-44d4-a61c-faaa8a989580,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"So systolic failure is referred to as HFREF, but what started as a problem emptying the heart has led to congestion and has produced a problem getting blood into the heart. Let us compare this with diastolic failure.",True,Ejection Fraction in Systolic Failure,,,,
b02c9910-a4b5-4294-90f2-691c1516a9d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,Ejection Fraction in Diastolic Failure,False,Ejection Fraction in Diastolic Failure,,,,
3442f51a-490a-4781-9c51-a7c00f795fe2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Remember that in diastolic failure there is a problem relaxing/filling the ventricle. Consequently EDV tends to be lower than normal, and this lower volume of blood in the chamber is relatively easy for the heart to expel. So proportionately, the ejection fraction can be maintained, even if the absolute stroke volume may be low. This is now classified as heart failure with a normal ejection fraction (HFNEF).",True,Ejection Fraction in Diastolic Failure,,,,
23b0e9b2-d72d-4f3d-afbc-184af4f18ffb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"The pathophysiological consequences of HFNEF stem from the poor relaxation of the ventricle and/or ability to accept blood. When the ventricle is noncompliant during diastole (i.e., does not relax properly), it does not take much blood volume to enter the chamber before the ventricle pressure begins to rise. This rise in ventricular pressure opposes the entry of more blood, so it accumulates in the atrium. Atrial pressure rises and venous return is impeded, so blood becomes congested in the venous system.",True,Ejection Fraction in Diastolic Failure,,,,
3898f0ed-8aff-4362-a573-2fd516b916c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
3898f0ed-8aff-4362-a573-2fd516b916c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
3898f0ed-8aff-4362-a573-2fd516b916c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
3898f0ed-8aff-4362-a573-2fd516b916c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
3898f0ed-8aff-4362-a573-2fd516b916c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
25a50977-1565-45b6-b163-8d56cc24662a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,True,Ejection Fraction in Diastolic Failure,,,,
bbd49dad-e940-4eed-abab-c9c2eb6ee326,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Initial responses to the diminished cardiac output include the acute compensatory responses to low blood pressure, myocardial stretch, or changes in renal perfusion. Let us do a quick review.",True,Ejection Fraction in Diastolic Failure,,,,
3ff32a5f-8210-4f73-a7d1-be6acdf8fea0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"The reduced cardiac output leads to a reduced arterial blood pressure, which, in combination with low volume exiting the heart, results in lower blood flow. With less blood exiting the heart, more remains in the chamber, particularly with systolic failure, so the myocardium is stretched. These three factors (pressure, flow, and myocardial stretch) elicit mechanical, neural, and hormone responses intended to correct the fall in pressure, resume flow, and clear the heart of congestion—but these responses are intended for a normal heart, not one undergoing failure.",True,Ejection Fraction in Diastolic Failure,,,,
f9a9c23f-11c6-4117-b84b-3f309b4eec58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
f9a9c23f-11c6-4117-b84b-3f309b4eec58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
f9a9c23f-11c6-4117-b84b-3f309b4eec58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
f9a9c23f-11c6-4117-b84b-3f309b4eec58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
f9a9c23f-11c6-4117-b84b-3f309b4eec58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
0487afdf-5450-4d55-b1e7-61e719b3fd0d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"These compensatory effects are all attempts to improve cardiac output and blood pressure, but the failing heart is being forced to work harder against an increased afterload and move more volume. Consequently, but for the natriuretic peptides, these responses are maladaptive in the long term, and chronic changes to the heart are instigated.",True,Ejection Fraction in Diastolic Failure,,,,
eea19fe5-eb09-4cba-b92e-e6c4acf18741,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,Chronic Remodeling and Hypertrophy,False,Chronic Remodeling and Hypertrophy,,,,
45754e5e-3f29-4f9e-982d-53b748f4b065,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"The long-term structural changes begin with additional wall stress in the failing heart interacting with neurohormonal and cytokine alterations, but the wall stress seems to be an important instigator of hypertrophy and remodeling. Stress can be placed on the chamber walls in two major ways.",True,Chronic Remodeling and Hypertrophy,,,,
982d4086-ecb5-4898-b023-2658f6fd35b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
982d4086-ecb5-4898-b023-2658f6fd35b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
982d4086-ecb5-4898-b023-2658f6fd35b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
982d4086-ecb5-4898-b023-2658f6fd35b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
982d4086-ecb5-4898-b023-2658f6fd35b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
43c320dc-89a9-4a13-99c1-08da7c28f803,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
43c320dc-89a9-4a13-99c1-08da7c28f803,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
43c320dc-89a9-4a13-99c1-08da7c28f803,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
43c320dc-89a9-4a13-99c1-08da7c28f803,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
43c320dc-89a9-4a13-99c1-08da7c28f803,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
b079cc8b-3d23-4749-8a17-3a83ec680918,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
b079cc8b-3d23-4749-8a17-3a83ec680918,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
b079cc8b-3d23-4749-8a17-3a83ec680918,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
b079cc8b-3d23-4749-8a17-3a83ec680918,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
b079cc8b-3d23-4749-8a17-3a83ec680918,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
8faac653-a05f-4bc3-a6ba-53c25337c768,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Myocytes may also be lost through either apoptosis or necrosis. As hypertrophy occurs the blood supply to the thickening wall becomes inadequate so infarction and consequent necrosis are more likely. Factors that promote myocyte apoptosis are all present during heart failure and include elevated catecholamines, Angiotensin II, inflammatory cytokines, and wall stress.",True,Chronic Remodeling and Hypertrophy,,,,
e5633249-dde0-456f-aecd-4bf2a88b0413,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"These same factors also disrupt gene expression in myocytes and cause intracellular deficits, including loss of Ca++ homeostasis and production of high-energy phosphates. While the mechanisms of these intracellular effects is still being heavily researched, the inability to control calcium or regulate high-energy phosphates obviously has implications of excitation–contraction coupling.",True,Chronic Remodeling and Hypertrophy,,,,
13846846-139b-47e4-8633-afe121e7edad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"So while hypertrophy may seem a sensible response in the failing heart, the patterns and inflammation and stress-driven changes are eventually maladaptive and lead to a progressive decline in cardiac function.",True,Chronic Remodeling and Hypertrophy,,,,
5e11b344-9a6e-4fae-a556-678828063b20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,Clinical Manifestations of Heart Failure,False,Clinical Manifestations of Heart Failure,,,,
3bb5c007-42c5-4fc5-a0fb-992170b3311d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
3bb5c007-42c5-4fc5-a0fb-992170b3311d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
3bb5c007-42c5-4fc5-a0fb-992170b3311d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
3bb5c007-42c5-4fc5-a0fb-992170b3311d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
3bb5c007-42c5-4fc5-a0fb-992170b3311d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
8ffad08b-c4d9-487b-81f8-119489378054,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"If the right heart fails, there is a rise in systemic venous pressure and peripheral edema arises. There may be abdominal discomfort as the liver becomes engorged and a loss of appetite or nausea as gastrointestinal edema arises. If the left heart fails, then the pulmonary circulation is exposed to the congestion and pulmonary edema arises.",True,Clinical Manifestations of Heart Failure,,,,
d9a16340-bd2f-4e9b-a92c-1e56987b46ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Low cardiac output reduces renal filtration, so urine formation maybe impaired. Similarly cerebral blood flow may be compromised, causing dulled mental status.",True,Clinical Manifestations of Heart Failure,,,,
fea8f30a-625a-4093-a460-32caeb1bed33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Orthopnea arises when the patient lays down and venous return toward the failing left ventricle increases, compounding the pulmonary congestion. Patients often sleep propped up on pillows to elevate the heart and lungs. In severe cases the patient may only be able to sleep upright in a chair.",True,Clinical Manifestations of Heart Failure,,,,
b94db7e9-fd40-46c9-b74c-cdf4f52fc598,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,Text,False,Text,,,,
29669ce8-f2d5-49a1-9e8d-a90cfb5ec626,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Eberly, Lauren A., Eldrin F. Lewis, and Leonard S. Lilly. “Heart Failure.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e, edited by Leonard S. Lilly, Chapter 9. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
2590cb56-200a-4b98-a906-4c7baa58774f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/#chapter-26-section-1,"Malik, Ahmad, Daniel Brito, Sarosh Vaqar, and Lovely Chhabra. Congestive Heart Failure. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430873/, CC BY 4.0.",True,Text,,,,
d735362a-4306-4a5b-bcbd-1ecb0ac1c9a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"For whichever reason the end effect of the failure is a decline in blood flow out of the heart, and consequently congestion on the way in.",True,Text,,,,
2770026b-a74b-4eac-8376-198778077d10,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,Table 2.1: Changes in cardiac function in different disease states.,True,Text,,,,
abe206cd-ba59-4720-ac6a-fac603926fdb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
abe206cd-ba59-4720-ac6a-fac603926fdb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
abe206cd-ba59-4720-ac6a-fac603926fdb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
abe206cd-ba59-4720-ac6a-fac603926fdb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
abe206cd-ba59-4720-ac6a-fac603926fdb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Impediments to emptying the heart during systole (i.e., a reduced contractility or increased afterload) were referred to as systolic heart failure. Similarly, problems with filling the ventricle during diastole were referred to as diastolic heart failure (figure 2.1).",True,Text,Figure 2.1,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.1-new-scaled.jpg,Figure 2.1: Overly simplified schema of heart failure. Systolic = cannot get the blood out; Diastolic = cannot get the blood in.
9688572d-daf1-4285-b2c1-56f7aaebb020,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"In reality there is a great deal of overlap between these forms of heart failure, and elements of both can be present in the same patient. Similarly, as both forms result in congestion before the heart and reduced flow after it, they are hard to immediately distinguish. Consequently the type and degree of failure is now categorized by the effect on ejection fraction that can help distinguish the source of the problem.",True,Text,,,,
4a909682-0ab0-4d0d-94e4-0e34a8e4989d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
4a909682-0ab0-4d0d-94e4-0e34a8e4989d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
4a909682-0ab0-4d0d-94e4-0e34a8e4989d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
4a909682-0ab0-4d0d-94e4-0e34a8e4989d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
4a909682-0ab0-4d0d-94e4-0e34a8e4989d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Let us quickly remind ourselves of what ejection fraction is. Ejection fraction is the proportion of blood volume that the left ventricle ejects in one beat. It is mathematically described as the starting volume (i.e., end-diastolic volume, EDV) minus the finishing volume (i.e., end-systolic volume, ESV) as a proportion of the starting volume (figure 2.2)—in simpler terms, what percentage of the ventricular blood volume was pushed out during a contraction.",True,Text,Figure 2.2,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.2-scaled.jpg,Figure 2.2: Calculation for ejection fraction.
e0cb07e5-738e-4b06-bc4a-1b0f8d1fc91e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,Ejection Fraction in Systolic Failure,False,Ejection Fraction in Systolic Failure,,,,
36e2671d-b31b-4680-9436-8e7387fa4215,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Let us first relate this to systolic failure by looking at what happens when the contractility of the myocardium is reduced. In systolic failure, there is a problem getting blood out of the heart, so the volume of blood coming out of the heart per beat (EDV-ESV) is reduced. However, the end diastolic volume will remain the same, or more likely rise. So our ejection fraction is reduced. Consequently, if you have a reduced ejection fraction you know you have a systolic failure. So to improve diagnosis, systolic failure is now referred to as heart failure with a reduced ejection fraction (HFREF).",True,Ejection Fraction in Systolic Failure,,,,
35797dcd-bf9d-47b0-b85e-734fae7ac8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
35797dcd-bf9d-47b0-b85e-734fae7ac8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
35797dcd-bf9d-47b0-b85e-734fae7ac8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
35797dcd-bf9d-47b0-b85e-734fae7ac8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
35797dcd-bf9d-47b0-b85e-734fae7ac8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Let us look at the pathophysiological consequences of HFREF. With a poor ejection fraction blood will begin to accumulate in the ventricle, and EDV will begins to rise and consequently so will the ventricular pressure. The raised pressure will impede venous return and promote venous congestion as blood struggles to enter the heart, and in the case of left ventricular failure the congestion will occur first in the left atrium and then in the pulmonary system (figure 2.3).",True,Ejection Fraction in Systolic Failure,Figure 2.3,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
c358f4a6-7e2b-41f2-a713-b799c4cb6504,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"So systolic failure is referred to as HFREF, but what started as a problem emptying the heart has led to congestion and has produced a problem getting blood into the heart. Let us compare this with diastolic failure.",True,Ejection Fraction in Systolic Failure,,,,
0a64d46b-e110-465a-9318-692f8846fd4f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,Ejection Fraction in Diastolic Failure,False,Ejection Fraction in Diastolic Failure,,,,
02ef6594-0d03-4f54-bc74-40b55c137f6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Remember that in diastolic failure there is a problem relaxing/filling the ventricle. Consequently EDV tends to be lower than normal, and this lower volume of blood in the chamber is relatively easy for the heart to expel. So proportionately, the ejection fraction can be maintained, even if the absolute stroke volume may be low. This is now classified as heart failure with a normal ejection fraction (HFNEF).",True,Ejection Fraction in Diastolic Failure,,,,
4d5cb734-5be3-4a63-867c-7ab71794bdbf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"The pathophysiological consequences of HFNEF stem from the poor relaxation of the ventricle and/or ability to accept blood. When the ventricle is noncompliant during diastole (i.e., does not relax properly), it does not take much blood volume to enter the chamber before the ventricle pressure begins to rise. This rise in ventricular pressure opposes the entry of more blood, so it accumulates in the atrium. Atrial pressure rises and venous return is impeded, so blood becomes congested in the venous system.",True,Ejection Fraction in Diastolic Failure,,,,
775ffc3d-1ded-4641-ab1b-a2be4eb60ded,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
775ffc3d-1ded-4641-ab1b-a2be4eb60ded,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
775ffc3d-1ded-4641-ab1b-a2be4eb60ded,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
775ffc3d-1ded-4641-ab1b-a2be4eb60ded,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
775ffc3d-1ded-4641-ab1b-a2be4eb60ded,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"If you compare this sequence of events in HFREF and HFNEF in figure 2.3 the end point is the same—congestion in the venous system, hence the difficulty in distinguishing “systolic” and “diastolic” failure and the need to measure ejection fraction and the newer categories of HFREF and HFNEF. In summary, HFREF starts with a problem getting blood out, that leads to a problem getting blood in, whereas HFNEF starts with a problem getting blood in that leads to a problem getting blood out. Both produce congestion, and both result in a diminished cardiac output.",True,Ejection Fraction in Diastolic Failure,Figure 2.3,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.3-new.png,"Figure 2.3: Pathophysiological sequence of left ventricular failure. Whether through lowered ejection fraction (HFREF, a.k.a. systolic failure) or through poor ventricular filling (heart failure with a normal ejection fraction, or HFNEF, a.k.a. diastolic failure), the end point of pulmonary congestion is the same."
1039091e-b572-4223-9011-622fc6c4bf56,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,True,Ejection Fraction in Diastolic Failure,,,,
fd39c46f-19b0-473d-a47e-14f9104c9d81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Initial responses to the diminished cardiac output include the acute compensatory responses to low blood pressure, myocardial stretch, or changes in renal perfusion. Let us do a quick review.",True,Ejection Fraction in Diastolic Failure,,,,
afb7dc1a-bcdc-4bd4-8bbd-1bf7e35e84a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"The reduced cardiac output leads to a reduced arterial blood pressure, which, in combination with low volume exiting the heart, results in lower blood flow. With less blood exiting the heart, more remains in the chamber, particularly with systolic failure, so the myocardium is stretched. These three factors (pressure, flow, and myocardial stretch) elicit mechanical, neural, and hormone responses intended to correct the fall in pressure, resume flow, and clear the heart of congestion—but these responses are intended for a normal heart, not one undergoing failure.",True,Ejection Fraction in Diastolic Failure,,,,
b66cb3d7-70aa-4d22-aef3-5d22184e054e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
b66cb3d7-70aa-4d22-aef3-5d22184e054e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
b66cb3d7-70aa-4d22-aef3-5d22184e054e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
b66cb3d7-70aa-4d22-aef3-5d22184e054e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
b66cb3d7-70aa-4d22-aef3-5d22184e054e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"First, the extended myocardium elicits the Frank-Starling mechanism to increase contractility, while the release of ANP and BNP induces sodium and fluid loss at the kidney. Conversely, reduced renal blood flow instigates the RAAS system to cause salt and fluid retention and vasoconstriction aided by the release of Endothelin-1 from the endothelium of flow-deprived vessels. Finally, the reduced arterial pressure prompts the baroreceptor reflex that increases sympathetic tone to increase rate and contractility, and antidiuretic hormone causes fluid retention. See the summary in figure 2.4.",True,Ejection Fraction in Diastolic Failure,Figure 2.4,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.4-new-scaled.jpg,Figure 2.4: Compensatory responses to reduced cardiac output.
49aeb213-8508-4417-85ba-f0b05c7cb9ab,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"These compensatory effects are all attempts to improve cardiac output and blood pressure, but the failing heart is being forced to work harder against an increased afterload and move more volume. Consequently, but for the natriuretic peptides, these responses are maladaptive in the long term, and chronic changes to the heart are instigated.",True,Ejection Fraction in Diastolic Failure,,,,
6930fe3a-7547-4270-a3ba-42367424fe4f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,Chronic Remodeling and Hypertrophy,False,Chronic Remodeling and Hypertrophy,,,,
ce2907ac-7f33-4ac1-9190-d7d986dde561,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"The long-term structural changes begin with additional wall stress in the failing heart interacting with neurohormonal and cytokine alterations, but the wall stress seems to be an important instigator of hypertrophy and remodeling. Stress can be placed on the chamber walls in two major ways.",True,Chronic Remodeling and Hypertrophy,,,,
20c37768-c9b7-4cb7-835f-ca6df0e70dc9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
20c37768-c9b7-4cb7-835f-ca6df0e70dc9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
20c37768-c9b7-4cb7-835f-ca6df0e70dc9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
20c37768-c9b7-4cb7-835f-ca6df0e70dc9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
20c37768-c9b7-4cb7-835f-ca6df0e70dc9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"But the two forms of overload (volume and pressure) lead to different patterns of hypertrophy. In volume overload the myocytes add more sarcomeres in series, so they elongate and contribute to the dilation of the chamber while there is a proportional increase in wall thickness. This is referred to as eccentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
d74ef50f-dcb5-4156-92e1-610ecc9381d4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
d74ef50f-dcb5-4156-92e1-610ecc9381d4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
d74ef50f-dcb5-4156-92e1-610ecc9381d4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
d74ef50f-dcb5-4156-92e1-610ecc9381d4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
d74ef50f-dcb5-4156-92e1-610ecc9381d4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Pressure loading, on the other hand, leads to the synthesis of new sarcomeres that are formed in parallel to the old ones, causing an increase in wall thickness without any dilation of the chamber. This is referred to as concentric hypertrophy (figure 2.5).",True,Chronic Remodeling and Hypertrophy,Figure 2.5,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.5-scaled.jpg,Figure 2.5: The effects of volume and pressure overload on the morphology of the heart and cardiac myocytes.
f036b933-f4a7-425b-9311-e68d9f4392e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
f036b933-f4a7-425b-9311-e68d9f4392e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
f036b933-f4a7-425b-9311-e68d9f4392e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
f036b933-f4a7-425b-9311-e68d9f4392e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
f036b933-f4a7-425b-9311-e68d9f4392e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,These adaptations are accompanied by increased deposition of connective tissue that may have conductive or contractive ramifications. The difference in myocytic arrangement and presence of connective tissue is clear in the histological views of normal myocardium and myocardium chronically exposed to valvular disease in figure 2.6.,True,Chronic Remodeling and Hypertrophy,Figure 2.6,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/2.6-scaled.jpg,Figure 2.6: Normal myocardial (A) and myocardium exposed to valvular disease (B).
e2aeab02-8858-4248-96b7-eb7d49c858ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Myocytes may also be lost through either apoptosis or necrosis. As hypertrophy occurs the blood supply to the thickening wall becomes inadequate so infarction and consequent necrosis are more likely. Factors that promote myocyte apoptosis are all present during heart failure and include elevated catecholamines, Angiotensin II, inflammatory cytokines, and wall stress.",True,Chronic Remodeling and Hypertrophy,,,,
2870bbf5-20d8-4eb2-941b-431a17886a25,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"These same factors also disrupt gene expression in myocytes and cause intracellular deficits, including loss of Ca++ homeostasis and production of high-energy phosphates. While the mechanisms of these intracellular effects is still being heavily researched, the inability to control calcium or regulate high-energy phosphates obviously has implications of excitation–contraction coupling.",True,Chronic Remodeling and Hypertrophy,,,,
6b728daa-6cc4-4bbd-9d07-e32e8acff234,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"So while hypertrophy may seem a sensible response in the failing heart, the patterns and inflammation and stress-driven changes are eventually maladaptive and lead to a progressive decline in cardiac function.",True,Chronic Remodeling and Hypertrophy,,,,
243950e9-ca7a-4a68-ac9a-975bc9fd7d56,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,Clinical Manifestations of Heart Failure,False,Clinical Manifestations of Heart Failure,,,,
24cdb701-034d-4c76-bfd1-86c381c9e531,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,Clinical Manifestations of Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
24cdb701-034d-4c76-bfd1-86c381c9e531,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,Chronic Remodeling and Hypertrophy,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
24cdb701-034d-4c76-bfd1-86c381c9e531,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,Acute Responses to Reduced Cardiac Output in Heart Failure: Good or Bad?,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
24cdb701-034d-4c76-bfd1-86c381c9e531,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,Heart Failure and Ejection Fraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
24cdb701-034d-4c76-bfd1-86c381c9e531,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,The clinical manifestations arise as fluid begins to move from the blood to the interstitium due to congestion (see summary in figure 2.7).,True,Clinical Manifestations of Heart Failure,Figure 2.7,2. Heart Failure,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2021/12/2.7-new.png,Figure 2.7: Consequences of right- and left-sided heart failure.
3776e3b2-0fea-4aac-acc5-681b094a316f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"If the right heart fails, there is a rise in systemic venous pressure and peripheral edema arises. There may be abdominal discomfort as the liver becomes engorged and a loss of appetite or nausea as gastrointestinal edema arises. If the left heart fails, then the pulmonary circulation is exposed to the congestion and pulmonary edema arises.",True,Clinical Manifestations of Heart Failure,,,,
6ffb1855-ead4-4e7d-baad-cc233841b0a1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Low cardiac output reduces renal filtration, so urine formation maybe impaired. Similarly cerebral blood flow may be compromised, causing dulled mental status.",True,Clinical Manifestations of Heart Failure,,,,
abc6027d-a2af-46b1-846d-a39721e4b1ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Orthopnea arises when the patient lays down and venous return toward the failing left ventricle increases, compounding the pulmonary congestion. Patients often sleep propped up on pillows to elevate the heart and lungs. In severe cases the patient may only be able to sleep upright in a chair.",True,Clinical Manifestations of Heart Failure,,,,
05f94e8d-3f19-42a2-aa66-a5f9a3a4fafe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,Text,False,Text,,,,
2f12bef9-71b1-4f72-a828-061a61218aeb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Eberly, Lauren A., Eldrin F. Lewis, and Leonard S. Lilly. “Heart Failure.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e, edited by Leonard S. Lilly, Chapter 9. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
fada3473-fc4c-4072-b6c9-a24a6119e035,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,2. Heart Failure,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-2-heart-failure/,"Malik, Ahmad, Daniel Brito, Sarosh Vaqar, and Lovely Chhabra. Congestive Heart Failure. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK430873/, CC BY 4.0.",True,Text,,,,
6c46f5ba-cd4b-46df-be9b-4a6f16ed3be2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,USMLE,False,USMLE,,,,
77eb1c38-43b0-47d4-96c7-3a2c17c4056c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
77eb1c38-43b0-47d4-96c7-3a2c17c4056c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
77eb1c38-43b0-47d4-96c7-3a2c17c4056c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
77eb1c38-43b0-47d4-96c7-3a2c17c4056c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
77eb1c38-43b0-47d4-96c7-3a2c17c4056c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
77eb1c38-43b0-47d4-96c7-3a2c17c4056c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
77eb1c38-43b0-47d4-96c7-3a2c17c4056c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
77eb1c38-43b0-47d4-96c7-3a2c17c4056c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
77eb1c38-43b0-47d4-96c7-3a2c17c4056c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
77eb1c38-43b0-47d4-96c7-3a2c17c4056c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
77eb1c38-43b0-47d4-96c7-3a2c17c4056c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
77eb1c38-43b0-47d4-96c7-3a2c17c4056c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
77eb1c38-43b0-47d4-96c7-3a2c17c4056c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
77eb1c38-43b0-47d4-96c7-3a2c17c4056c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
77eb1c38-43b0-47d4-96c7-3a2c17c4056c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
77eb1c38-43b0-47d4-96c7-3a2c17c4056c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
77eb1c38-43b0-47d4-96c7-3a2c17c4056c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f46b72ef-06f9-4563-bda4-c278a237fa2f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,10q22,False,10q22,,,,
b8793902-7452-426b-96d7-a119cd75ef71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,q24,False,q24,,,,
7027c49e-bf8b-4d34-9d4f-0a51df267154,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,fibrillatory,False,fibrillatory,,,,
3aee9c75-9844-4eed-9724-f09cc605c6ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3aee9c75-9844-4eed-9724-f09cc605c6ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3aee9c75-9844-4eed-9724-f09cc605c6ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3aee9c75-9844-4eed-9724-f09cc605c6ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3aee9c75-9844-4eed-9724-f09cc605c6ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3aee9c75-9844-4eed-9724-f09cc605c6ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3aee9c75-9844-4eed-9724-f09cc605c6ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3aee9c75-9844-4eed-9724-f09cc605c6ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3aee9c75-9844-4eed-9724-f09cc605c6ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3aee9c75-9844-4eed-9724-f09cc605c6ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3aee9c75-9844-4eed-9724-f09cc605c6ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3aee9c75-9844-4eed-9724-f09cc605c6ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3aee9c75-9844-4eed-9724-f09cc605c6ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3aee9c75-9844-4eed-9724-f09cc605c6ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3aee9c75-9844-4eed-9724-f09cc605c6ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3aee9c75-9844-4eed-9724-f09cc605c6ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3aee9c75-9844-4eed-9724-f09cc605c6ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
639d540a-0158-4f7d-9820-e67b5789ff80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Table 1.1: Atrial fibrillation summary.,True,fibrillatory,,,,
178f8b4b-2f2d-47c8-a4d9-92fe0b874e4f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Atrial Flutter,False,Atrial Flutter,,,,
818acd74-546e-4e12-9767-de1f0f024d58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
818acd74-546e-4e12-9767-de1f0f024d58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
818acd74-546e-4e12-9767-de1f0f024d58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
818acd74-546e-4e12-9767-de1f0f024d58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
818acd74-546e-4e12-9767-de1f0f024d58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
818acd74-546e-4e12-9767-de1f0f024d58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
818acd74-546e-4e12-9767-de1f0f024d58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
818acd74-546e-4e12-9767-de1f0f024d58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
818acd74-546e-4e12-9767-de1f0f024d58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
818acd74-546e-4e12-9767-de1f0f024d58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
818acd74-546e-4e12-9767-de1f0f024d58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
818acd74-546e-4e12-9767-de1f0f024d58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
818acd74-546e-4e12-9767-de1f0f024d58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
818acd74-546e-4e12-9767-de1f0f024d58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
818acd74-546e-4e12-9767-de1f0f024d58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
818acd74-546e-4e12-9767-de1f0f024d58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
818acd74-546e-4e12-9767-de1f0f024d58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
7901f6d3-4a4f-47c1-b2f3-ed60b1bcaab5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,macroreentrant,False,macroreentrant,,,,
3082a6e8-a32b-486c-84f2-37181b801cfa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,cavotricuspid,False,cavotricuspid,,,,
f7916563-e0d7-45f6-801c-c44dbb0572db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"As with atrial fibrillation, the AV node’s refractory period prevents most of the P-waves from progressing to the ventricle, but commonly the AV conduction will be 2-to-1, so with an atrial rate of 300 bpm the ventricular rate will be 150 bpm. Parasympathetic stimulation or changes in AV node refractoriness can modify how many P-waves pass into the ventricle, but the the resultant rhythm is “regularly irregular.” When the heart rate is elevated, then distinguishing flutter from fibrillation becomes challenging and slowing ventricular rate pharmaceutically (adenosine) helps the flutter waves reemerge for a definitive diagnosis to be made.",True,cavotricuspid,,,,
ae040685-4088-4ccd-b7e7-8ae11993a0e8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Table 1.2: Atrial flutter summary.,True,cavotricuspid,,,,
6af9e4b1-ef83-4de9-923d-7c09cba52590,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Multifocal Atrial Tachycardia,False,Multifocal Atrial Tachycardia,,,,
af0d299e-2b3f-4089-b62a-9764b4a18f71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
af0d299e-2b3f-4089-b62a-9764b4a18f71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
af0d299e-2b3f-4089-b62a-9764b4a18f71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
af0d299e-2b3f-4089-b62a-9764b4a18f71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
af0d299e-2b3f-4089-b62a-9764b4a18f71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
af0d299e-2b3f-4089-b62a-9764b4a18f71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
af0d299e-2b3f-4089-b62a-9764b4a18f71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
af0d299e-2b3f-4089-b62a-9764b4a18f71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
af0d299e-2b3f-4089-b62a-9764b4a18f71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
af0d299e-2b3f-4089-b62a-9764b4a18f71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
af0d299e-2b3f-4089-b62a-9764b4a18f71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
af0d299e-2b3f-4089-b62a-9764b4a18f71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
af0d299e-2b3f-4089-b62a-9764b4a18f71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
af0d299e-2b3f-4089-b62a-9764b4a18f71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
af0d299e-2b3f-4089-b62a-9764b4a18f71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
af0d299e-2b3f-4089-b62a-9764b4a18f71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
af0d299e-2b3f-4089-b62a-9764b4a18f71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
69d51e67-954b-4217-ad36-a22a50989d54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"MAT frequently occurs in the setting of severe lung disease and, more specifically, during an exacerbation of lung disease. This rhythm is benign, and once the underlying lung disease is treated, it should resolve.",True,Multifocal Atrial Tachycardia,,,,
98afd1fa-85df-4d62-a0c1-9e9c898401fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Table 1.3: MAT summary.,True,Multifocal Atrial Tachycardia,,,,
4cba9425-2ae2-4564-b06d-4dbc63fd3b2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Premature Atrial Contraction,False,Premature Atrial Contraction,,,,
8bb9a3f4-eda3-41e3-bdac-aecaedc793cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A premature atrial contraction (PAC) is generated by a depolarization instigated outside of the SA node. This produces an extra P-wave, and consequently a shortening from previous P-P intervals is seen. The aberrant P-wave also has a different morphology from a sinus P-wave because of its different anatomical origin.",True,Premature Atrial Contraction,,,,
7d84a37a-b966-4fe7-808c-348e93346e99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d84a37a-b966-4fe7-808c-348e93346e99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d84a37a-b966-4fe7-808c-348e93346e99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d84a37a-b966-4fe7-808c-348e93346e99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d84a37a-b966-4fe7-808c-348e93346e99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d84a37a-b966-4fe7-808c-348e93346e99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d84a37a-b966-4fe7-808c-348e93346e99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d84a37a-b966-4fe7-808c-348e93346e99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d84a37a-b966-4fe7-808c-348e93346e99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d84a37a-b966-4fe7-808c-348e93346e99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d84a37a-b966-4fe7-808c-348e93346e99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d84a37a-b966-4fe7-808c-348e93346e99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d84a37a-b966-4fe7-808c-348e93346e99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d84a37a-b966-4fe7-808c-348e93346e99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d84a37a-b966-4fe7-808c-348e93346e99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d84a37a-b966-4fe7-808c-348e93346e99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d84a37a-b966-4fe7-808c-348e93346e99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
37713deb-c7b3-4fbc-b01c-3eb0aaa9d84c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"If a PAC occurs when the AV node has not yet recovered from its refractory period, the PAC will fail to conduct to the ventricles; meaning the PAC will not be followed by a QRS complex or the ectopic P-R interval will be prolonged. The ECG will show a premature, ectopic P-wave and then no QRS complex afterward. When this occurs along with bigeminy, the ECG can appear as if there is sinus bradycardia.",True,Premature Atrial Contraction,,,,
2b9aed14-4aa1-4521-9f3c-275cf0a91144,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Table 1.4: PAC summary.,True,Premature Atrial Contraction,,,,
10e603ab-8f39-46fa-b0bf-7d92fc3221e0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Sinus Bradycardia,False,Sinus Bradycardia,,,,
c51217b8-d2af-458e-9418-7fbedc1cfabc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Sinus bradycardia denotes a sinus rhythm below 60 bpm. Otherwise the ECG waveform is normal on an ECG with an upright P-wave in lead II preceding every QRS complex. There are many intrinsic causes associated with the heart itself, as well as extrinsic causes, some of which are listed table 1.5. Sinus bradycardia is usually asymptomatic as rates of 40–50 bpm can maintain hemodynamic stability. Rates below this can produce symptoms of fatigue, dizziness, and dyspnea on exertion.",True,Sinus Bradycardia,,,,
971cfd9a-1095-4b66-9155-ceda21053890,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Table 1.5: Intrinsic and extrinsic causes associated with the heart.,True,Sinus Bradycardia,,,,
fd17df84-794f-4519-a7eb-53390b52b442,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Table 1.6: Sinus bradycardia summary.,True,Sinus Bradycardia,,,,
9effc782-cdd4-42f2-8f31-d6b9d6ee0ed2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Premature Ventricular Contractions,False,Premature Ventricular Contractions,,,,
dc9ee840-69de-4976-87b6-7abde5e38a90,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
dc9ee840-69de-4976-87b6-7abde5e38a90,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
dc9ee840-69de-4976-87b6-7abde5e38a90,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
dc9ee840-69de-4976-87b6-7abde5e38a90,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
dc9ee840-69de-4976-87b6-7abde5e38a90,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
dc9ee840-69de-4976-87b6-7abde5e38a90,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
dc9ee840-69de-4976-87b6-7abde5e38a90,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
dc9ee840-69de-4976-87b6-7abde5e38a90,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
dc9ee840-69de-4976-87b6-7abde5e38a90,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
dc9ee840-69de-4976-87b6-7abde5e38a90,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
dc9ee840-69de-4976-87b6-7abde5e38a90,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
dc9ee840-69de-4976-87b6-7abde5e38a90,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
dc9ee840-69de-4976-87b6-7abde5e38a90,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
dc9ee840-69de-4976-87b6-7abde5e38a90,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
dc9ee840-69de-4976-87b6-7abde5e38a90,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
dc9ee840-69de-4976-87b6-7abde5e38a90,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
dc9ee840-69de-4976-87b6-7abde5e38a90,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
23079878-bc12-424c-9e14-a9826f400b5b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Table 1.7: PVC summary.,True,Premature Ventricular Contractions,,,,
28557e1f-119f-4244-815b-027c7e462e4f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Ventricular Tachycardia,False,Ventricular Tachycardia,,,,
0ee66a98-cebd-476f-99fb-3bd440a76037,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Ventricular tachycardia (VT) is caused by reentry currents being established in the ventricular myocardium or groups of ventricular myocytes that have aberrant electrical behavior. As such, VT is usually caused by underlying cardiac disease.",True,Ventricular Tachycardia,,,,
c446e254-69fd-477f-b95e-d85d69a4a7bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Like a PVC, the aberrant depolarizations do not follow the normal conduction pathways so are wide (>120 msecs), but unlike a PVC, VT involves a ventricular rate >100 bpm. With disorganized contractility and reduced filling time, VT can lead to hemodynamic instability and severe hypotension—hence it is life threatening.",True,Ventricular Tachycardia,,,,
740e2583-adaa-4879-9900-42e40e3469ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The QRS morphology in VT is highly variable between patients and depends on where the arrhythmia originates. Consequently there are several ways to classify VT based on duration, symptoms, QRS morphology, rate, and origin.",True,Ventricular Tachycardia,,,,
c3cb9d9f-2d2b-4cfe-8810-58f2fa676d70,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Sustained VT is any VT that lasts for more than 30 seconds or is symptomatic. Nonsustained VT lasts for less than 30 seconds and is asymptomatic.,True,Ventricular Tachycardia,,,,
404d4366-865a-4d38-8585-bbc56474a36d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
404d4366-865a-4d38-8585-bbc56474a36d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
404d4366-865a-4d38-8585-bbc56474a36d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
404d4366-865a-4d38-8585-bbc56474a36d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
404d4366-865a-4d38-8585-bbc56474a36d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
404d4366-865a-4d38-8585-bbc56474a36d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
404d4366-865a-4d38-8585-bbc56474a36d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
404d4366-865a-4d38-8585-bbc56474a36d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
404d4366-865a-4d38-8585-bbc56474a36d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
404d4366-865a-4d38-8585-bbc56474a36d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
404d4366-865a-4d38-8585-bbc56474a36d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
404d4366-865a-4d38-8585-bbc56474a36d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
404d4366-865a-4d38-8585-bbc56474a36d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
404d4366-865a-4d38-8585-bbc56474a36d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
404d4366-865a-4d38-8585-bbc56474a36d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
404d4366-865a-4d38-8585-bbc56474a36d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
404d4366-865a-4d38-8585-bbc56474a36d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
4e92395d-61e7-40e7-b3bd-de21c9a0c006,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
4e92395d-61e7-40e7-b3bd-de21c9a0c006,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
4e92395d-61e7-40e7-b3bd-de21c9a0c006,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
4e92395d-61e7-40e7-b3bd-de21c9a0c006,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
4e92395d-61e7-40e7-b3bd-de21c9a0c006,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
4e92395d-61e7-40e7-b3bd-de21c9a0c006,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
4e92395d-61e7-40e7-b3bd-de21c9a0c006,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
4e92395d-61e7-40e7-b3bd-de21c9a0c006,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
4e92395d-61e7-40e7-b3bd-de21c9a0c006,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
4e92395d-61e7-40e7-b3bd-de21c9a0c006,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
4e92395d-61e7-40e7-b3bd-de21c9a0c006,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
4e92395d-61e7-40e7-b3bd-de21c9a0c006,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
4e92395d-61e7-40e7-b3bd-de21c9a0c006,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
4e92395d-61e7-40e7-b3bd-de21c9a0c006,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
4e92395d-61e7-40e7-b3bd-de21c9a0c006,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
4e92395d-61e7-40e7-b3bd-de21c9a0c006,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
4e92395d-61e7-40e7-b3bd-de21c9a0c006,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
4165fe0e-c783-42fb-9b63-edc7c4a8c906,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Torsades de pointes is associated with a prolonged QT interval (>600 msecs) that helps distinguish it from other forms of polymorphous VT. The longer QT interval can be caused by ionic abnormalities that reduce the repolarizing current of Phase 3 of the cardiac action potential. This makes the myocardium susceptible to early after-depolarizations—the trigger for torsades de pointes. These after-depolarizations do not happen uniformly across the myocardium and are more common in endocardial tissue where the repolarization currents are slower. So torsades de pointes arises from the after-depolarizations causing reentry currents in neighboring tissue.,True,Ventricular Tachycardia,,,,
44532f18-cc77-412b-9a9f-8e896baa0e7c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Both common garden variety VTs and torsades de pointes can progress to ventricular fibrillation.,True,Ventricular Tachycardia,,,,
f04b8ce2-30d4-4391-bb46-71176695b350,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Table 1.8: VT summary.,True,Ventricular Tachycardia,,,,
05c698a0-3c11-49f2-9b45-f762a4ecdd4c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Ventricular Fibrillation,False,Ventricular Fibrillation,,,,
33e8af1d-efa7-4fd2-98e0-85c264cccead,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Ventricular fibrillation (VF) occurs when the ventricular rate exceeds 400 bpm. The disorganized and uncoordinated contraction of the myocardium causes cardiac output to fall to catastrophic levels. Rates of survival for out-of-hospital VF are low.,True,Ventricular Fibrillation,,,,
01764ee2-2aa5-4abb-899c-572d11954a23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
01764ee2-2aa5-4abb-899c-572d11954a23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
01764ee2-2aa5-4abb-899c-572d11954a23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
01764ee2-2aa5-4abb-899c-572d11954a23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
01764ee2-2aa5-4abb-899c-572d11954a23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
01764ee2-2aa5-4abb-899c-572d11954a23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
01764ee2-2aa5-4abb-899c-572d11954a23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
01764ee2-2aa5-4abb-899c-572d11954a23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
01764ee2-2aa5-4abb-899c-572d11954a23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
01764ee2-2aa5-4abb-899c-572d11954a23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
01764ee2-2aa5-4abb-899c-572d11954a23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
01764ee2-2aa5-4abb-899c-572d11954a23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
01764ee2-2aa5-4abb-899c-572d11954a23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
01764ee2-2aa5-4abb-899c-572d11954a23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
01764ee2-2aa5-4abb-899c-572d11954a23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
01764ee2-2aa5-4abb-899c-572d11954a23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
01764ee2-2aa5-4abb-899c-572d11954a23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
21fd698f-b39d-40ea-9c6a-ae7c5d2c7faf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Table 1.9: VF summary.,True,Ventricular Fibrillation,,,,
9b4f91e0-801b-4631-ba6d-d02525b927e8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,First-Degree Atrioventricular Block,False,First-Degree Atrioventricular Block,,,,
26fd284b-1d08-488e-addc-2f1d278c835d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
26fd284b-1d08-488e-addc-2f1d278c835d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
26fd284b-1d08-488e-addc-2f1d278c835d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
26fd284b-1d08-488e-addc-2f1d278c835d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
26fd284b-1d08-488e-addc-2f1d278c835d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
26fd284b-1d08-488e-addc-2f1d278c835d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
26fd284b-1d08-488e-addc-2f1d278c835d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
26fd284b-1d08-488e-addc-2f1d278c835d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
26fd284b-1d08-488e-addc-2f1d278c835d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
26fd284b-1d08-488e-addc-2f1d278c835d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
26fd284b-1d08-488e-addc-2f1d278c835d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
26fd284b-1d08-488e-addc-2f1d278c835d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
26fd284b-1d08-488e-addc-2f1d278c835d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
26fd284b-1d08-488e-addc-2f1d278c835d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
26fd284b-1d08-488e-addc-2f1d278c835d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
26fd284b-1d08-488e-addc-2f1d278c835d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
26fd284b-1d08-488e-addc-2f1d278c835d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
c0c80220-7953-4f14-aa25-f18009fc23d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
c0c80220-7953-4f14-aa25-f18009fc23d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
c0c80220-7953-4f14-aa25-f18009fc23d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
c0c80220-7953-4f14-aa25-f18009fc23d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
c0c80220-7953-4f14-aa25-f18009fc23d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
c0c80220-7953-4f14-aa25-f18009fc23d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
c0c80220-7953-4f14-aa25-f18009fc23d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
c0c80220-7953-4f14-aa25-f18009fc23d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
c0c80220-7953-4f14-aa25-f18009fc23d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
c0c80220-7953-4f14-aa25-f18009fc23d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
c0c80220-7953-4f14-aa25-f18009fc23d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
c0c80220-7953-4f14-aa25-f18009fc23d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
c0c80220-7953-4f14-aa25-f18009fc23d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
c0c80220-7953-4f14-aa25-f18009fc23d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
c0c80220-7953-4f14-aa25-f18009fc23d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
c0c80220-7953-4f14-aa25-f18009fc23d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
c0c80220-7953-4f14-aa25-f18009fc23d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
c743fff8-73b7-4075-a969-1feae0d8a568,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Table 1.10: First-degree block summary.,True,First-Degree Atrioventricular Block,,,,
de2cec40-73b4-4f8d-91b4-f9ef35abdaa2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Second-Degree Atrioventricular Block,False,Second-Degree Atrioventricular Block,,,,
df09dbda-3d2e-4c9b-8b12-c7c7c05b4acb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A second-degree atrioventricular block also has changes in P-R interval, but it starts to show failure of the P-wave to propagate a QRS complex every time (i.e., intermittently the depolarization fails to reach the ventricles). The pattern of missed ventricular depolarizations, or blocked P-waves, is often very regular and described as a ratio of P-waves to QRS complex. The way in which the P-R interval changes in relation to the blocked P-waves produces subclassifications of second-degree blocks, Mobitz I and II.",True,Second-Degree Atrioventricular Block,,,,
f9d26c65-3284-41a0-b2ad-4b66547da199,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9d26c65-3284-41a0-b2ad-4b66547da199,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9d26c65-3284-41a0-b2ad-4b66547da199,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9d26c65-3284-41a0-b2ad-4b66547da199,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9d26c65-3284-41a0-b2ad-4b66547da199,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9d26c65-3284-41a0-b2ad-4b66547da199,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9d26c65-3284-41a0-b2ad-4b66547da199,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9d26c65-3284-41a0-b2ad-4b66547da199,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9d26c65-3284-41a0-b2ad-4b66547da199,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9d26c65-3284-41a0-b2ad-4b66547da199,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9d26c65-3284-41a0-b2ad-4b66547da199,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9d26c65-3284-41a0-b2ad-4b66547da199,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9d26c65-3284-41a0-b2ad-4b66547da199,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9d26c65-3284-41a0-b2ad-4b66547da199,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9d26c65-3284-41a0-b2ad-4b66547da199,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9d26c65-3284-41a0-b2ad-4b66547da199,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9d26c65-3284-41a0-b2ad-4b66547da199,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
48fe1443-e99b-4d7a-ad87-78d36e7557b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
48fe1443-e99b-4d7a-ad87-78d36e7557b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
48fe1443-e99b-4d7a-ad87-78d36e7557b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
48fe1443-e99b-4d7a-ad87-78d36e7557b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
48fe1443-e99b-4d7a-ad87-78d36e7557b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
48fe1443-e99b-4d7a-ad87-78d36e7557b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
48fe1443-e99b-4d7a-ad87-78d36e7557b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
48fe1443-e99b-4d7a-ad87-78d36e7557b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
48fe1443-e99b-4d7a-ad87-78d36e7557b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
48fe1443-e99b-4d7a-ad87-78d36e7557b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
48fe1443-e99b-4d7a-ad87-78d36e7557b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
48fe1443-e99b-4d7a-ad87-78d36e7557b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
48fe1443-e99b-4d7a-ad87-78d36e7557b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
48fe1443-e99b-4d7a-ad87-78d36e7557b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
48fe1443-e99b-4d7a-ad87-78d36e7557b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
48fe1443-e99b-4d7a-ad87-78d36e7557b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
48fe1443-e99b-4d7a-ad87-78d36e7557b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a1642ccd-4cff-4d8a-9308-edf4c700436d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Table 1.11: Second-degree block summary.,True,Second-Degree Atrioventricular Block,,,,
a4608bf3-06e9-47e8-8006-55d25793936f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Third-Degree Atrioventricular Block,False,Third-Degree Atrioventricular Block,,,,
61b944f1-ad84-4652-aadc-89ed8cf18352,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
61b944f1-ad84-4652-aadc-89ed8cf18352,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
61b944f1-ad84-4652-aadc-89ed8cf18352,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
61b944f1-ad84-4652-aadc-89ed8cf18352,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
61b944f1-ad84-4652-aadc-89ed8cf18352,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
61b944f1-ad84-4652-aadc-89ed8cf18352,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
61b944f1-ad84-4652-aadc-89ed8cf18352,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
61b944f1-ad84-4652-aadc-89ed8cf18352,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
61b944f1-ad84-4652-aadc-89ed8cf18352,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
61b944f1-ad84-4652-aadc-89ed8cf18352,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
61b944f1-ad84-4652-aadc-89ed8cf18352,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
61b944f1-ad84-4652-aadc-89ed8cf18352,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
61b944f1-ad84-4652-aadc-89ed8cf18352,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
61b944f1-ad84-4652-aadc-89ed8cf18352,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
61b944f1-ad84-4652-aadc-89ed8cf18352,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
61b944f1-ad84-4652-aadc-89ed8cf18352,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
61b944f1-ad84-4652-aadc-89ed8cf18352,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
190d3598-0b72-47c6-9ef7-0547c20cfca4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Table 1.12: Third-degree block summary.,True,Third-Degree Atrioventricular Block,,,,
4bc7df69-7264-4d65-a3f7-76203dcef9ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Left Bundle Branch Block,False,Left Bundle Branch Block,,,,
7d8c7572-df90-4f8b-9ce4-756804698c77,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"A left bundle branch block (LBBB) is generated when the conductivity of the His-Purkinje system in the left ventricle is compromised, either through damage or disease. The ECG changes, and criteria for LBBB relate to these changes in conductivity and the left-side location.",True,Left Bundle Branch Block,,,,
d816de31-6a21-4de3-a05e-28301d77ae86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
d816de31-6a21-4de3-a05e-28301d77ae86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
d816de31-6a21-4de3-a05e-28301d77ae86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
d816de31-6a21-4de3-a05e-28301d77ae86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
d816de31-6a21-4de3-a05e-28301d77ae86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
d816de31-6a21-4de3-a05e-28301d77ae86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
d816de31-6a21-4de3-a05e-28301d77ae86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
d816de31-6a21-4de3-a05e-28301d77ae86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
d816de31-6a21-4de3-a05e-28301d77ae86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
d816de31-6a21-4de3-a05e-28301d77ae86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
d816de31-6a21-4de3-a05e-28301d77ae86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
d816de31-6a21-4de3-a05e-28301d77ae86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
d816de31-6a21-4de3-a05e-28301d77ae86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
d816de31-6a21-4de3-a05e-28301d77ae86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
d816de31-6a21-4de3-a05e-28301d77ae86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
d816de31-6a21-4de3-a05e-28301d77ae86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
d816de31-6a21-4de3-a05e-28301d77ae86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ea861933-f312-44a7-b370-ce8f7bcfde6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The lateral leads (I, V5, and V6) normally show a downward deflecting Q-wave as normal septal deflection initially occurs left-to-right (i.e., away from the lateral leads). In LBBB the change in direction to right-to-left, plus the longer duration, eliminates the Q-wave from the lateral leads, and Q-waves will be small in aVL.",True,Left Bundle Branch Block,,,,
2080c0ff-56d1-4e29-8db3-51cc8f868100,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
2080c0ff-56d1-4e29-8db3-51cc8f868100,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
2080c0ff-56d1-4e29-8db3-51cc8f868100,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
2080c0ff-56d1-4e29-8db3-51cc8f868100,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
2080c0ff-56d1-4e29-8db3-51cc8f868100,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
2080c0ff-56d1-4e29-8db3-51cc8f868100,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
2080c0ff-56d1-4e29-8db3-51cc8f868100,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
2080c0ff-56d1-4e29-8db3-51cc8f868100,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
2080c0ff-56d1-4e29-8db3-51cc8f868100,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
2080c0ff-56d1-4e29-8db3-51cc8f868100,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
2080c0ff-56d1-4e29-8db3-51cc8f868100,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
2080c0ff-56d1-4e29-8db3-51cc8f868100,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
2080c0ff-56d1-4e29-8db3-51cc8f868100,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
2080c0ff-56d1-4e29-8db3-51cc8f868100,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
2080c0ff-56d1-4e29-8db3-51cc8f868100,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
2080c0ff-56d1-4e29-8db3-51cc8f868100,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
2080c0ff-56d1-4e29-8db3-51cc8f868100,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
a1da0307-b435-4784-be2c-4eac84a16ecc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a1da0307-b435-4784-be2c-4eac84a16ecc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a1da0307-b435-4784-be2c-4eac84a16ecc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a1da0307-b435-4784-be2c-4eac84a16ecc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a1da0307-b435-4784-be2c-4eac84a16ecc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a1da0307-b435-4784-be2c-4eac84a16ecc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a1da0307-b435-4784-be2c-4eac84a16ecc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a1da0307-b435-4784-be2c-4eac84a16ecc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a1da0307-b435-4784-be2c-4eac84a16ecc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a1da0307-b435-4784-be2c-4eac84a16ecc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a1da0307-b435-4784-be2c-4eac84a16ecc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a1da0307-b435-4784-be2c-4eac84a16ecc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a1da0307-b435-4784-be2c-4eac84a16ecc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a1da0307-b435-4784-be2c-4eac84a16ecc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a1da0307-b435-4784-be2c-4eac84a16ecc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a1da0307-b435-4784-be2c-4eac84a16ecc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a1da0307-b435-4784-be2c-4eac84a16ecc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
e92edea7-e190-4049-ba98-e1f1633e591f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Table 1.13: LBBB summary.,True,Left Bundle Branch Block,,,,
051c8ca1-b15e-42d1-8361-5aed91faa6da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Right Bundle Branch Block,False,Right Bundle Branch Block,,,,
205b49ac-17ce-43c1-aacd-68e3d026a96b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The causes and manifestations of a right bundle branch block (RBBB) bear some similarities to those described for LBBB, but of course this time its depolarization of the right ventricle is delayed. Causes of RBBB include ischemic heart disease again as well as other myocardial diseases, but pulmonary issues such as pulmonary embolism and cor pulmonale can be added to the list.",True,Right Bundle Branch Block,,,,
421580b1-f84f-4e74-96ce-fc2031991d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
421580b1-f84f-4e74-96ce-fc2031991d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
421580b1-f84f-4e74-96ce-fc2031991d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
421580b1-f84f-4e74-96ce-fc2031991d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
421580b1-f84f-4e74-96ce-fc2031991d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
421580b1-f84f-4e74-96ce-fc2031991d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
421580b1-f84f-4e74-96ce-fc2031991d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
421580b1-f84f-4e74-96ce-fc2031991d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
421580b1-f84f-4e74-96ce-fc2031991d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
421580b1-f84f-4e74-96ce-fc2031991d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
421580b1-f84f-4e74-96ce-fc2031991d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
421580b1-f84f-4e74-96ce-fc2031991d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
421580b1-f84f-4e74-96ce-fc2031991d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
421580b1-f84f-4e74-96ce-fc2031991d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
421580b1-f84f-4e74-96ce-fc2031991d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
421580b1-f84f-4e74-96ce-fc2031991d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
421580b1-f84f-4e74-96ce-fc2031991d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
fe029546-fd85-41f4-8858-24dfa01f1d67,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Table 1.14: RBBB summary.,True,Right Bundle Branch Block,,,,
f1574f5a-6c63-4d63-b842-e538a4fe50a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Wolff-Parkinson-White Syndrome,False,Wolff-Parkinson-White Syndrome,,,,
330caca1-1db9-4ae4-9ff4-9452e5516814,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Normally the only electrical connection between the atria and the ventricles is the AV node. Otherwise the fibrous skeleton of the heart electrically insulates the atria from the ventricles. In Wolff-Parkinson-White (WPW) syndrome, that insulation is incomplete, and an “accessory pathway” connects the electrical system of the atria directly to the ventricles. If you think of the AV node as a bridge over the fibrous wall with regulated access, the accessory pathway is like a pathological tunnel under it with no regulation.",True,Wolff-Parkinson-White Syndrome,,,,
2e85d51e-4ad4-4591-8ff6-5d386e5cced4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
2e85d51e-4ad4-4591-8ff6-5d386e5cced4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
2e85d51e-4ad4-4591-8ff6-5d386e5cced4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
2e85d51e-4ad4-4591-8ff6-5d386e5cced4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
2e85d51e-4ad4-4591-8ff6-5d386e5cced4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
2e85d51e-4ad4-4591-8ff6-5d386e5cced4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
2e85d51e-4ad4-4591-8ff6-5d386e5cced4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
2e85d51e-4ad4-4591-8ff6-5d386e5cced4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
2e85d51e-4ad4-4591-8ff6-5d386e5cced4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
2e85d51e-4ad4-4591-8ff6-5d386e5cced4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
2e85d51e-4ad4-4591-8ff6-5d386e5cced4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
2e85d51e-4ad4-4591-8ff6-5d386e5cced4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
2e85d51e-4ad4-4591-8ff6-5d386e5cced4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
2e85d51e-4ad4-4591-8ff6-5d386e5cced4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
2e85d51e-4ad4-4591-8ff6-5d386e5cced4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
2e85d51e-4ad4-4591-8ff6-5d386e5cced4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
2e85d51e-4ad4-4591-8ff6-5d386e5cced4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
cb95c23f-df1f-4ad6-9ae3-5dcf0a4ade4d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"WPW syndrome is often asymptomatic, and patients do not require immediate treatment. However, if atrial fibrillation occurs in a WPW patient, the accessory pathway can allow the atrial fibrillation waves through to the ventricle (with no AV nodal refractory period to prevent them). Consequently a high ventricular rate is seen, and the risk of ventricular fibrillation being established means immediate clinical attention is required.",True,Wolff-Parkinson-White Syndrome,,,,
3035e5d9-c887-40f5-aedc-3082e70604f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Hyper- and Hypocalcemia,False,Hyper- and Hypocalcemia,,,,
38c72953-09f5-4d7b-8d42-b09066da831a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
38c72953-09f5-4d7b-8d42-b09066da831a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
38c72953-09f5-4d7b-8d42-b09066da831a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
38c72953-09f5-4d7b-8d42-b09066da831a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
38c72953-09f5-4d7b-8d42-b09066da831a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
38c72953-09f5-4d7b-8d42-b09066da831a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
38c72953-09f5-4d7b-8d42-b09066da831a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
38c72953-09f5-4d7b-8d42-b09066da831a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
38c72953-09f5-4d7b-8d42-b09066da831a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
38c72953-09f5-4d7b-8d42-b09066da831a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
38c72953-09f5-4d7b-8d42-b09066da831a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
38c72953-09f5-4d7b-8d42-b09066da831a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
38c72953-09f5-4d7b-8d42-b09066da831a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
38c72953-09f5-4d7b-8d42-b09066da831a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
38c72953-09f5-4d7b-8d42-b09066da831a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
38c72953-09f5-4d7b-8d42-b09066da831a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
38c72953-09f5-4d7b-8d42-b09066da831a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
63b671b1-8b99-4cdb-b28f-24b3e8fc25b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
63b671b1-8b99-4cdb-b28f-24b3e8fc25b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
63b671b1-8b99-4cdb-b28f-24b3e8fc25b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
63b671b1-8b99-4cdb-b28f-24b3e8fc25b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
63b671b1-8b99-4cdb-b28f-24b3e8fc25b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
63b671b1-8b99-4cdb-b28f-24b3e8fc25b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
63b671b1-8b99-4cdb-b28f-24b3e8fc25b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
63b671b1-8b99-4cdb-b28f-24b3e8fc25b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
63b671b1-8b99-4cdb-b28f-24b3e8fc25b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
63b671b1-8b99-4cdb-b28f-24b3e8fc25b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
63b671b1-8b99-4cdb-b28f-24b3e8fc25b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
63b671b1-8b99-4cdb-b28f-24b3e8fc25b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
63b671b1-8b99-4cdb-b28f-24b3e8fc25b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
63b671b1-8b99-4cdb-b28f-24b3e8fc25b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
63b671b1-8b99-4cdb-b28f-24b3e8fc25b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
63b671b1-8b99-4cdb-b28f-24b3e8fc25b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
63b671b1-8b99-4cdb-b28f-24b3e8fc25b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
fefcffa4-b8dc-4ef8-a8c2-701e5e9afbe3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Table 1.16: Hyper- and hypocalcemia summary.,True,Hyper- and Hypocalcemia,,,,
61c5760f-25de-49b1-b522-3dece56df2cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Hyper- and Hypokalemia,False,Hyper- and Hypokalemia,,,,
a06e32f7-e9ee-43af-9582-869eb8490ff4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"The pathophysiology is not as simple as changes in extracellular K+ changing the electrochemical gradient for K+. Because of potassium’s role in maintaining the resting membrane potential, shifts in extracellular potassium can also influence the activity of Na+ and Ca++ channels.",True,Hyper- and Hypokalemia,,,,
2667f29a-a755-4a38-985d-d706f37adaba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2667f29a-a755-4a38-985d-d706f37adaba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2667f29a-a755-4a38-985d-d706f37adaba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2667f29a-a755-4a38-985d-d706f37adaba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2667f29a-a755-4a38-985d-d706f37adaba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2667f29a-a755-4a38-985d-d706f37adaba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2667f29a-a755-4a38-985d-d706f37adaba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2667f29a-a755-4a38-985d-d706f37adaba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2667f29a-a755-4a38-985d-d706f37adaba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2667f29a-a755-4a38-985d-d706f37adaba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2667f29a-a755-4a38-985d-d706f37adaba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2667f29a-a755-4a38-985d-d706f37adaba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2667f29a-a755-4a38-985d-d706f37adaba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2667f29a-a755-4a38-985d-d706f37adaba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2667f29a-a755-4a38-985d-d706f37adaba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2667f29a-a755-4a38-985d-d706f37adaba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2667f29a-a755-4a38-985d-d706f37adaba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
37c842fb-78a5-4e08-a063-339d8ef14949,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"As hypokalemia also inhibits Na+-K+ ATPase, Na+ accumulates inside the cell. This in turn leads to an accumulation of Ca++ because of a subsequent failure of the Na+-Ca++ exchanger. Extended presence of these two positive ions inside the myocyte prolongs the action potential and may manifest as an increased width and amplitude of the P-wave.",True,Hyper- and Hypokalemia,,,,
76f1e8bf-2c73-4b0a-89b6-b9ba772253a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"As hypokalemia worsens, the problems with K+ conductance and repolarization increase, and the myocardium becomes susceptible to early after-depolarization (EAD) arrhythmias.",True,Hyper- and Hypokalemia,,,,
a52d120f-fd2e-4cd2-b407-63069bdc1796,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a52d120f-fd2e-4cd2-b407-63069bdc1796,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a52d120f-fd2e-4cd2-b407-63069bdc1796,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a52d120f-fd2e-4cd2-b407-63069bdc1796,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a52d120f-fd2e-4cd2-b407-63069bdc1796,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a52d120f-fd2e-4cd2-b407-63069bdc1796,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a52d120f-fd2e-4cd2-b407-63069bdc1796,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a52d120f-fd2e-4cd2-b407-63069bdc1796,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a52d120f-fd2e-4cd2-b407-63069bdc1796,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a52d120f-fd2e-4cd2-b407-63069bdc1796,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a52d120f-fd2e-4cd2-b407-63069bdc1796,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a52d120f-fd2e-4cd2-b407-63069bdc1796,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a52d120f-fd2e-4cd2-b407-63069bdc1796,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a52d120f-fd2e-4cd2-b407-63069bdc1796,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a52d120f-fd2e-4cd2-b407-63069bdc1796,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a52d120f-fd2e-4cd2-b407-63069bdc1796,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a52d120f-fd2e-4cd2-b407-63069bdc1796,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fbfd6120-fe57-4551-99a2-1931c696dee2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fbfd6120-fe57-4551-99a2-1931c696dee2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fbfd6120-fe57-4551-99a2-1931c696dee2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fbfd6120-fe57-4551-99a2-1931c696dee2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fbfd6120-fe57-4551-99a2-1931c696dee2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fbfd6120-fe57-4551-99a2-1931c696dee2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fbfd6120-fe57-4551-99a2-1931c696dee2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fbfd6120-fe57-4551-99a2-1931c696dee2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fbfd6120-fe57-4551-99a2-1931c696dee2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fbfd6120-fe57-4551-99a2-1931c696dee2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fbfd6120-fe57-4551-99a2-1931c696dee2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fbfd6120-fe57-4551-99a2-1931c696dee2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fbfd6120-fe57-4551-99a2-1931c696dee2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fbfd6120-fe57-4551-99a2-1931c696dee2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fbfd6120-fe57-4551-99a2-1931c696dee2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fbfd6120-fe57-4551-99a2-1931c696dee2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fbfd6120-fe57-4551-99a2-1931c696dee2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
b8e21e93-ae09-4953-9220-de2a123f5fc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8e21e93-ae09-4953-9220-de2a123f5fc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8e21e93-ae09-4953-9220-de2a123f5fc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8e21e93-ae09-4953-9220-de2a123f5fc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8e21e93-ae09-4953-9220-de2a123f5fc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8e21e93-ae09-4953-9220-de2a123f5fc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8e21e93-ae09-4953-9220-de2a123f5fc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8e21e93-ae09-4953-9220-de2a123f5fc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8e21e93-ae09-4953-9220-de2a123f5fc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8e21e93-ae09-4953-9220-de2a123f5fc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8e21e93-ae09-4953-9220-de2a123f5fc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8e21e93-ae09-4953-9220-de2a123f5fc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8e21e93-ae09-4953-9220-de2a123f5fc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8e21e93-ae09-4953-9220-de2a123f5fc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8e21e93-ae09-4953-9220-de2a123f5fc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8e21e93-ae09-4953-9220-de2a123f5fc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8e21e93-ae09-4953-9220-de2a123f5fc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
97d5700a-306c-4745-90d8-94d723590dea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97d5700a-306c-4745-90d8-94d723590dea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97d5700a-306c-4745-90d8-94d723590dea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97d5700a-306c-4745-90d8-94d723590dea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97d5700a-306c-4745-90d8-94d723590dea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97d5700a-306c-4745-90d8-94d723590dea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97d5700a-306c-4745-90d8-94d723590dea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97d5700a-306c-4745-90d8-94d723590dea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97d5700a-306c-4745-90d8-94d723590dea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97d5700a-306c-4745-90d8-94d723590dea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97d5700a-306c-4745-90d8-94d723590dea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97d5700a-306c-4745-90d8-94d723590dea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97d5700a-306c-4745-90d8-94d723590dea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97d5700a-306c-4745-90d8-94d723590dea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97d5700a-306c-4745-90d8-94d723590dea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97d5700a-306c-4745-90d8-94d723590dea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97d5700a-306c-4745-90d8-94d723590dea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
2f0edb5d-c677-4289-bf39-55bb65e19c52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Table 1.17: Hypo- and hyperkalemia summary.,True,Hyper- and Hypokalemia,,,,
db70c622-ab24-4c25-ae89-2675ffd7083d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"References, resources, and further reading",False,"References, resources, and further reading",,,,
116c7bb2-c667-474c-a0da-fc4101b3d4c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,Text,False,Text,,,,
25e09e1a-9d83-488d-ad5f-1fbe028f8fb0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Burns, Ed, and Robert Buttner. Hypercalcaemia. Lift in the Fast Lane, 2021. https://litfl.com/hypercalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
98b0eb2b-328b-4f37-95d0-4a1d717348c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Burns, Ed, and Robert Buttner. Hypocalcaemia. Life in the Fast Lane, 2021. https://litfl.com/hypocalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
924eb71e-f15c-45cf-a207-17b43a28255e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Buttner, Robert, and Ed Burns. Hyperkalaemia. Life in the Fast Lane. https://litfl.com/hyperkalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
3f6b51a5-0594-4ad0-aff0-def446f6da9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Buttner, Robert, and Ed Burns. Hypokalaemia. Life in the Fast Lane, 2021. https://litfl.com/hypokalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
c2ec9ebd-39e6-4027-8d33-99309d013968,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Chhabra, Lovely, Amandeep Goyal, and Michael D. Benham. Wolff Parkinson White Syndrome. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK554437/, CC BY 4.0.",True,Text,,,,
de0f5e7f-54b2-4ef7-80ca-92553b8b6171,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Custer, Adam M., Varun S. Yelamanchili, and Sarah L. Lappin. Multifocal Atrial Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459152/, CC BY 4.0.",True,Text,,,,
3e262579-d93b-409b-983d-96ddc6f0517c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Farzam, Khashayar, and John R. Richards. Premature Ventricular Contraction. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532991/, CC BY 4.0.",True,Text,,,,
7328f663-c5ef-4e2f-ade4-a4211caf5868,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Foth, Christopher, Manesh Kumar Gangwani, and Heidi Alvey. Ventricular Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532954/, CC BY 4.0.",True,Text,,,,
fc065c88-8e7e-4e26-a309-85650123fb33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Hafeez, Yamama, and Shamai A. Grossman. Sinus Bradycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK493201/, CC BY 4.0.",True,Text,,,,
f1595d60-c9c3-4d6b-ba3b-44af48991758,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Harkness, Weston T., and Mary Hicks. Right Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK507872/, CC BY 4.0.",True,Text,,,,
d2624d0f-ba5a-421e-b634-e2a663b7ab7e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Heaton, Joseph, and Srikanth Yandrapalli. Premature Atrial Contractions. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK559204/, CC BY 4.0.",True,Text,,,,
dcf93591-9453-4b52-a6ad-1aca2b965dd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Kashou, Anthony H., Amandeep Goyal, Tran Nguyen, and Lovely Chhabra. Atrioventricular Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459147/, CC BY 4.0.",True,Text,,,,
54fd1955-7dcf-474e-a1c7-48be82daaf68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,“Learn the Heart.” Healio. https://www.healio.com/cardiology/learn-the-heart.,True,Text,,,,
d631c93d-f5f0-400a-84c4-7fbe032819dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Ludhwani, Dipesh, Amandeep Goyal, and Mandar Jagtap. Ventricular Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK537120/, CC BY 4.0.",True,Text,,,,
23d28e5a-2755-4f59-a997-fe25fb642627,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Nesheiwat, Zeid, Amandeep Goyal, and Mandar Jagtap. Atrial Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK526072/, CC BY 4.0.",True,Text,,,,
c652c067-fadb-4dcb-b5b7-c4507437ffd4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Pipilas, Daniel C., Bruce A. Koplan, and Leonard S. Lilly. “The Electrocardiogram.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 4. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
7c80cf5c-7fd6-4813-bb3d-279ddffa421e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Rodriguez Ziccardi, Mary, Amandeep Goyal, and Christopher V. Maani. Atrial Flutter. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK540985/, CC BY 4.0.",True,Text,,,,
9c33cea2-2522-4f34-b5de-1bb5ae1c0182,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-16,"Scherbak, Dmitriy, and Gregory J. Hicks. Left Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK482167/, CC BY 4.0.",True,Text,,,,
1bbbc589-eca4-453f-b218-ee21d1ecdf2e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,USMLE,False,USMLE,,,,
58deabbe-1789-4643-a3da-62c533e2e3b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
58deabbe-1789-4643-a3da-62c533e2e3b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
58deabbe-1789-4643-a3da-62c533e2e3b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
58deabbe-1789-4643-a3da-62c533e2e3b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
58deabbe-1789-4643-a3da-62c533e2e3b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
58deabbe-1789-4643-a3da-62c533e2e3b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
58deabbe-1789-4643-a3da-62c533e2e3b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
58deabbe-1789-4643-a3da-62c533e2e3b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
58deabbe-1789-4643-a3da-62c533e2e3b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
58deabbe-1789-4643-a3da-62c533e2e3b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
58deabbe-1789-4643-a3da-62c533e2e3b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
58deabbe-1789-4643-a3da-62c533e2e3b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
58deabbe-1789-4643-a3da-62c533e2e3b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
58deabbe-1789-4643-a3da-62c533e2e3b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
58deabbe-1789-4643-a3da-62c533e2e3b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
58deabbe-1789-4643-a3da-62c533e2e3b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
58deabbe-1789-4643-a3da-62c533e2e3b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
86ffdf6c-7e0b-4f98-9f9c-709b7c7a4d31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,10q22,False,10q22,,,,
825ce460-d94f-4a09-bad3-b42b1f3c86e8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,q24,False,q24,,,,
b812b14a-10a1-4c9e-a076-3bd40f4c0070,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,fibrillatory,False,fibrillatory,,,,
0e8e03b5-f9fe-4ab7-aa61-f7ef8c53451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
0e8e03b5-f9fe-4ab7-aa61-f7ef8c53451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
0e8e03b5-f9fe-4ab7-aa61-f7ef8c53451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
0e8e03b5-f9fe-4ab7-aa61-f7ef8c53451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
0e8e03b5-f9fe-4ab7-aa61-f7ef8c53451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
0e8e03b5-f9fe-4ab7-aa61-f7ef8c53451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
0e8e03b5-f9fe-4ab7-aa61-f7ef8c53451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
0e8e03b5-f9fe-4ab7-aa61-f7ef8c53451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
0e8e03b5-f9fe-4ab7-aa61-f7ef8c53451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
0e8e03b5-f9fe-4ab7-aa61-f7ef8c53451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
0e8e03b5-f9fe-4ab7-aa61-f7ef8c53451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
0e8e03b5-f9fe-4ab7-aa61-f7ef8c53451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
0e8e03b5-f9fe-4ab7-aa61-f7ef8c53451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
0e8e03b5-f9fe-4ab7-aa61-f7ef8c53451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
0e8e03b5-f9fe-4ab7-aa61-f7ef8c53451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
0e8e03b5-f9fe-4ab7-aa61-f7ef8c53451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
0e8e03b5-f9fe-4ab7-aa61-f7ef8c53451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
f466999e-1365-4263-95bd-e367de5fd803,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Table 1.1: Atrial fibrillation summary.,True,fibrillatory,,,,
c853195a-b79e-41cb-8056-451ed23726d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Atrial Flutter,False,Atrial Flutter,,,,
bd59f234-e9a0-47a6-91ce-5650e874f9c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bd59f234-e9a0-47a6-91ce-5650e874f9c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bd59f234-e9a0-47a6-91ce-5650e874f9c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bd59f234-e9a0-47a6-91ce-5650e874f9c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bd59f234-e9a0-47a6-91ce-5650e874f9c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bd59f234-e9a0-47a6-91ce-5650e874f9c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bd59f234-e9a0-47a6-91ce-5650e874f9c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bd59f234-e9a0-47a6-91ce-5650e874f9c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bd59f234-e9a0-47a6-91ce-5650e874f9c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bd59f234-e9a0-47a6-91ce-5650e874f9c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bd59f234-e9a0-47a6-91ce-5650e874f9c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bd59f234-e9a0-47a6-91ce-5650e874f9c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bd59f234-e9a0-47a6-91ce-5650e874f9c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bd59f234-e9a0-47a6-91ce-5650e874f9c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bd59f234-e9a0-47a6-91ce-5650e874f9c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bd59f234-e9a0-47a6-91ce-5650e874f9c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bd59f234-e9a0-47a6-91ce-5650e874f9c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
02431ab0-e190-4c18-9f2a-4158d2932aa1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,macroreentrant,False,macroreentrant,,,,
30f740df-8c55-4ed6-9ec2-fbc1a1f44917,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,cavotricuspid,False,cavotricuspid,,,,
90029db1-b9fe-4231-85e5-783ea330599e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"As with atrial fibrillation, the AV node’s refractory period prevents most of the P-waves from progressing to the ventricle, but commonly the AV conduction will be 2-to-1, so with an atrial rate of 300 bpm the ventricular rate will be 150 bpm. Parasympathetic stimulation or changes in AV node refractoriness can modify how many P-waves pass into the ventricle, but the the resultant rhythm is “regularly irregular.” When the heart rate is elevated, then distinguishing flutter from fibrillation becomes challenging and slowing ventricular rate pharmaceutically (adenosine) helps the flutter waves reemerge for a definitive diagnosis to be made.",True,cavotricuspid,,,,
630b0b3d-013b-4d94-a71e-70997dc2aae9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Table 1.2: Atrial flutter summary.,True,cavotricuspid,,,,
721a1808-44e4-413a-af36-33c8040e738d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Multifocal Atrial Tachycardia,False,Multifocal Atrial Tachycardia,,,,
a634b46f-f671-4886-a7fd-d44c94daf454,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a634b46f-f671-4886-a7fd-d44c94daf454,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a634b46f-f671-4886-a7fd-d44c94daf454,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a634b46f-f671-4886-a7fd-d44c94daf454,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a634b46f-f671-4886-a7fd-d44c94daf454,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a634b46f-f671-4886-a7fd-d44c94daf454,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a634b46f-f671-4886-a7fd-d44c94daf454,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a634b46f-f671-4886-a7fd-d44c94daf454,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a634b46f-f671-4886-a7fd-d44c94daf454,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a634b46f-f671-4886-a7fd-d44c94daf454,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a634b46f-f671-4886-a7fd-d44c94daf454,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a634b46f-f671-4886-a7fd-d44c94daf454,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a634b46f-f671-4886-a7fd-d44c94daf454,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a634b46f-f671-4886-a7fd-d44c94daf454,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a634b46f-f671-4886-a7fd-d44c94daf454,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a634b46f-f671-4886-a7fd-d44c94daf454,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a634b46f-f671-4886-a7fd-d44c94daf454,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
aa106d9d-775d-47d7-ac9a-a29854ca72d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"MAT frequently occurs in the setting of severe lung disease and, more specifically, during an exacerbation of lung disease. This rhythm is benign, and once the underlying lung disease is treated, it should resolve.",True,Multifocal Atrial Tachycardia,,,,
4cd8e000-4b6e-49b2-8ac3-413829868f49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Table 1.3: MAT summary.,True,Multifocal Atrial Tachycardia,,,,
6fb9fd8d-ef65-43d3-82a5-1b437e3805ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Premature Atrial Contraction,False,Premature Atrial Contraction,,,,
72928db9-548f-418c-864c-24a1c06ebb91,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A premature atrial contraction (PAC) is generated by a depolarization instigated outside of the SA node. This produces an extra P-wave, and consequently a shortening from previous P-P intervals is seen. The aberrant P-wave also has a different morphology from a sinus P-wave because of its different anatomical origin.",True,Premature Atrial Contraction,,,,
922c9c5e-68e2-447a-9fec-c020a83f293d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
922c9c5e-68e2-447a-9fec-c020a83f293d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
922c9c5e-68e2-447a-9fec-c020a83f293d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
922c9c5e-68e2-447a-9fec-c020a83f293d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
922c9c5e-68e2-447a-9fec-c020a83f293d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
922c9c5e-68e2-447a-9fec-c020a83f293d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
922c9c5e-68e2-447a-9fec-c020a83f293d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
922c9c5e-68e2-447a-9fec-c020a83f293d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
922c9c5e-68e2-447a-9fec-c020a83f293d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
922c9c5e-68e2-447a-9fec-c020a83f293d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
922c9c5e-68e2-447a-9fec-c020a83f293d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
922c9c5e-68e2-447a-9fec-c020a83f293d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
922c9c5e-68e2-447a-9fec-c020a83f293d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
922c9c5e-68e2-447a-9fec-c020a83f293d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
922c9c5e-68e2-447a-9fec-c020a83f293d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
922c9c5e-68e2-447a-9fec-c020a83f293d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
922c9c5e-68e2-447a-9fec-c020a83f293d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
297db643-af68-45c1-a513-30ab856c6477,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"If a PAC occurs when the AV node has not yet recovered from its refractory period, the PAC will fail to conduct to the ventricles; meaning the PAC will not be followed by a QRS complex or the ectopic P-R interval will be prolonged. The ECG will show a premature, ectopic P-wave and then no QRS complex afterward. When this occurs along with bigeminy, the ECG can appear as if there is sinus bradycardia.",True,Premature Atrial Contraction,,,,
2d1a7a60-dbcf-4f72-8988-a27cce06eaa0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Table 1.4: PAC summary.,True,Premature Atrial Contraction,,,,
3aad87a2-efca-403c-a971-8f8dc3354ca7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Sinus Bradycardia,False,Sinus Bradycardia,,,,
a0da63e1-b448-4dac-8997-2a70df10f5e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Sinus bradycardia denotes a sinus rhythm below 60 bpm. Otherwise the ECG waveform is normal on an ECG with an upright P-wave in lead II preceding every QRS complex. There are many intrinsic causes associated with the heart itself, as well as extrinsic causes, some of which are listed table 1.5. Sinus bradycardia is usually asymptomatic as rates of 40–50 bpm can maintain hemodynamic stability. Rates below this can produce symptoms of fatigue, dizziness, and dyspnea on exertion.",True,Sinus Bradycardia,,,,
ef0586a8-cc1f-4f79-89cd-6df08e850a4c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Table 1.5: Intrinsic and extrinsic causes associated with the heart.,True,Sinus Bradycardia,,,,
06aec50a-3f30-417e-861b-18c72e0239d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Table 1.6: Sinus bradycardia summary.,True,Sinus Bradycardia,,,,
fba04a74-ddf4-4098-b5ba-892c68d38cb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Premature Ventricular Contractions,False,Premature Ventricular Contractions,,,,
76690863-4587-4408-a425-aab258a75981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
76690863-4587-4408-a425-aab258a75981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
76690863-4587-4408-a425-aab258a75981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
76690863-4587-4408-a425-aab258a75981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
76690863-4587-4408-a425-aab258a75981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
76690863-4587-4408-a425-aab258a75981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
76690863-4587-4408-a425-aab258a75981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
76690863-4587-4408-a425-aab258a75981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
76690863-4587-4408-a425-aab258a75981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
76690863-4587-4408-a425-aab258a75981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
76690863-4587-4408-a425-aab258a75981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
76690863-4587-4408-a425-aab258a75981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
76690863-4587-4408-a425-aab258a75981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
76690863-4587-4408-a425-aab258a75981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
76690863-4587-4408-a425-aab258a75981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
76690863-4587-4408-a425-aab258a75981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
76690863-4587-4408-a425-aab258a75981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
91dd37f9-780d-49fe-b394-e17906fce346,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Table 1.7: PVC summary.,True,Premature Ventricular Contractions,,,,
02398e02-2bc5-4928-8512-2aef49b3f493,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Ventricular Tachycardia,False,Ventricular Tachycardia,,,,
d308d146-4dc4-4a74-9d55-40dfe75a76d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Ventricular tachycardia (VT) is caused by reentry currents being established in the ventricular myocardium or groups of ventricular myocytes that have aberrant electrical behavior. As such, VT is usually caused by underlying cardiac disease.",True,Ventricular Tachycardia,,,,
49725fbb-21f3-4612-b91c-051e49881abb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Like a PVC, the aberrant depolarizations do not follow the normal conduction pathways so are wide (>120 msecs), but unlike a PVC, VT involves a ventricular rate >100 bpm. With disorganized contractility and reduced filling time, VT can lead to hemodynamic instability and severe hypotension—hence it is life threatening.",True,Ventricular Tachycardia,,,,
85b0dbe4-5db5-4709-9d1e-68c390dff9c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The QRS morphology in VT is highly variable between patients and depends on where the arrhythmia originates. Consequently there are several ways to classify VT based on duration, symptoms, QRS morphology, rate, and origin.",True,Ventricular Tachycardia,,,,
8e5e91e1-04bf-4e6f-a4b8-92444008af63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Sustained VT is any VT that lasts for more than 30 seconds or is symptomatic. Nonsustained VT lasts for less than 30 seconds and is asymptomatic.,True,Ventricular Tachycardia,,,,
2ce7651a-e5f1-4a21-aba6-51f968d3d0b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
2ce7651a-e5f1-4a21-aba6-51f968d3d0b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
2ce7651a-e5f1-4a21-aba6-51f968d3d0b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
2ce7651a-e5f1-4a21-aba6-51f968d3d0b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
2ce7651a-e5f1-4a21-aba6-51f968d3d0b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
2ce7651a-e5f1-4a21-aba6-51f968d3d0b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
2ce7651a-e5f1-4a21-aba6-51f968d3d0b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
2ce7651a-e5f1-4a21-aba6-51f968d3d0b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
2ce7651a-e5f1-4a21-aba6-51f968d3d0b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
2ce7651a-e5f1-4a21-aba6-51f968d3d0b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
2ce7651a-e5f1-4a21-aba6-51f968d3d0b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
2ce7651a-e5f1-4a21-aba6-51f968d3d0b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
2ce7651a-e5f1-4a21-aba6-51f968d3d0b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
2ce7651a-e5f1-4a21-aba6-51f968d3d0b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
2ce7651a-e5f1-4a21-aba6-51f968d3d0b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
2ce7651a-e5f1-4a21-aba6-51f968d3d0b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
2ce7651a-e5f1-4a21-aba6-51f968d3d0b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
1fe0db98-0cff-488e-9e63-474d249a1f0a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
1fe0db98-0cff-488e-9e63-474d249a1f0a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
1fe0db98-0cff-488e-9e63-474d249a1f0a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
1fe0db98-0cff-488e-9e63-474d249a1f0a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
1fe0db98-0cff-488e-9e63-474d249a1f0a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
1fe0db98-0cff-488e-9e63-474d249a1f0a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
1fe0db98-0cff-488e-9e63-474d249a1f0a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
1fe0db98-0cff-488e-9e63-474d249a1f0a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
1fe0db98-0cff-488e-9e63-474d249a1f0a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
1fe0db98-0cff-488e-9e63-474d249a1f0a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
1fe0db98-0cff-488e-9e63-474d249a1f0a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
1fe0db98-0cff-488e-9e63-474d249a1f0a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
1fe0db98-0cff-488e-9e63-474d249a1f0a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
1fe0db98-0cff-488e-9e63-474d249a1f0a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
1fe0db98-0cff-488e-9e63-474d249a1f0a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
1fe0db98-0cff-488e-9e63-474d249a1f0a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
1fe0db98-0cff-488e-9e63-474d249a1f0a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
2abe5114-1a8e-45e2-85ab-3f8b12a8d2a3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Torsades de pointes is associated with a prolonged QT interval (>600 msecs) that helps distinguish it from other forms of polymorphous VT. The longer QT interval can be caused by ionic abnormalities that reduce the repolarizing current of Phase 3 of the cardiac action potential. This makes the myocardium susceptible to early after-depolarizations—the trigger for torsades de pointes. These after-depolarizations do not happen uniformly across the myocardium and are more common in endocardial tissue where the repolarization currents are slower. So torsades de pointes arises from the after-depolarizations causing reentry currents in neighboring tissue.,True,Ventricular Tachycardia,,,,
6158df82-2c83-4f92-8745-9bccb2a1bde7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Both common garden variety VTs and torsades de pointes can progress to ventricular fibrillation.,True,Ventricular Tachycardia,,,,
824e2f83-0b91-471a-8844-4a9a0bff74ff,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Table 1.8: VT summary.,True,Ventricular Tachycardia,,,,
3c1ec448-cb66-43b3-806b-e9ae99a9baf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Ventricular Fibrillation,False,Ventricular Fibrillation,,,,
88876c5a-71ef-4d9b-9bc4-2674249d332a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Ventricular fibrillation (VF) occurs when the ventricular rate exceeds 400 bpm. The disorganized and uncoordinated contraction of the myocardium causes cardiac output to fall to catastrophic levels. Rates of survival for out-of-hospital VF are low.,True,Ventricular Fibrillation,,,,
ef8ea4ce-ae4a-4ff3-bba7-f43fbde34418,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
ef8ea4ce-ae4a-4ff3-bba7-f43fbde34418,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
ef8ea4ce-ae4a-4ff3-bba7-f43fbde34418,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
ef8ea4ce-ae4a-4ff3-bba7-f43fbde34418,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
ef8ea4ce-ae4a-4ff3-bba7-f43fbde34418,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
ef8ea4ce-ae4a-4ff3-bba7-f43fbde34418,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
ef8ea4ce-ae4a-4ff3-bba7-f43fbde34418,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
ef8ea4ce-ae4a-4ff3-bba7-f43fbde34418,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
ef8ea4ce-ae4a-4ff3-bba7-f43fbde34418,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
ef8ea4ce-ae4a-4ff3-bba7-f43fbde34418,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
ef8ea4ce-ae4a-4ff3-bba7-f43fbde34418,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
ef8ea4ce-ae4a-4ff3-bba7-f43fbde34418,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
ef8ea4ce-ae4a-4ff3-bba7-f43fbde34418,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
ef8ea4ce-ae4a-4ff3-bba7-f43fbde34418,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
ef8ea4ce-ae4a-4ff3-bba7-f43fbde34418,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
ef8ea4ce-ae4a-4ff3-bba7-f43fbde34418,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
ef8ea4ce-ae4a-4ff3-bba7-f43fbde34418,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
c34c9b58-2364-4d33-a8b8-7898b8e8cbe3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Table 1.9: VF summary.,True,Ventricular Fibrillation,,,,
b3e8fbe7-10bb-45f7-8b33-5423ffcfb1e3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,First-Degree Atrioventricular Block,False,First-Degree Atrioventricular Block,,,,
6aea7291-3c90-425d-ad4a-af4c456d5821,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6aea7291-3c90-425d-ad4a-af4c456d5821,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6aea7291-3c90-425d-ad4a-af4c456d5821,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6aea7291-3c90-425d-ad4a-af4c456d5821,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6aea7291-3c90-425d-ad4a-af4c456d5821,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6aea7291-3c90-425d-ad4a-af4c456d5821,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6aea7291-3c90-425d-ad4a-af4c456d5821,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6aea7291-3c90-425d-ad4a-af4c456d5821,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6aea7291-3c90-425d-ad4a-af4c456d5821,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6aea7291-3c90-425d-ad4a-af4c456d5821,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6aea7291-3c90-425d-ad4a-af4c456d5821,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6aea7291-3c90-425d-ad4a-af4c456d5821,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6aea7291-3c90-425d-ad4a-af4c456d5821,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6aea7291-3c90-425d-ad4a-af4c456d5821,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6aea7291-3c90-425d-ad4a-af4c456d5821,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6aea7291-3c90-425d-ad4a-af4c456d5821,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6aea7291-3c90-425d-ad4a-af4c456d5821,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
b9f7a974-b5c5-4b18-8991-9d50e2879105,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
b9f7a974-b5c5-4b18-8991-9d50e2879105,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
b9f7a974-b5c5-4b18-8991-9d50e2879105,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
b9f7a974-b5c5-4b18-8991-9d50e2879105,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
b9f7a974-b5c5-4b18-8991-9d50e2879105,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
b9f7a974-b5c5-4b18-8991-9d50e2879105,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
b9f7a974-b5c5-4b18-8991-9d50e2879105,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
b9f7a974-b5c5-4b18-8991-9d50e2879105,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
b9f7a974-b5c5-4b18-8991-9d50e2879105,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
b9f7a974-b5c5-4b18-8991-9d50e2879105,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
b9f7a974-b5c5-4b18-8991-9d50e2879105,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
b9f7a974-b5c5-4b18-8991-9d50e2879105,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
b9f7a974-b5c5-4b18-8991-9d50e2879105,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
b9f7a974-b5c5-4b18-8991-9d50e2879105,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
b9f7a974-b5c5-4b18-8991-9d50e2879105,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
b9f7a974-b5c5-4b18-8991-9d50e2879105,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
b9f7a974-b5c5-4b18-8991-9d50e2879105,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
e7b284cc-5fe7-4042-a953-58d5bbb698c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Table 1.10: First-degree block summary.,True,First-Degree Atrioventricular Block,,,,
4706cca4-b98d-4e30-af7a-cc6229eeb633,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Second-Degree Atrioventricular Block,False,Second-Degree Atrioventricular Block,,,,
fae22b00-1e67-436a-88a9-d822b975a914,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A second-degree atrioventricular block also has changes in P-R interval, but it starts to show failure of the P-wave to propagate a QRS complex every time (i.e., intermittently the depolarization fails to reach the ventricles). The pattern of missed ventricular depolarizations, or blocked P-waves, is often very regular and described as a ratio of P-waves to QRS complex. The way in which the P-R interval changes in relation to the blocked P-waves produces subclassifications of second-degree blocks, Mobitz I and II.",True,Second-Degree Atrioventricular Block,,,,
965becd4-b0f7-4c4f-9ec4-c60c8c003146,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
965becd4-b0f7-4c4f-9ec4-c60c8c003146,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
965becd4-b0f7-4c4f-9ec4-c60c8c003146,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
965becd4-b0f7-4c4f-9ec4-c60c8c003146,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
965becd4-b0f7-4c4f-9ec4-c60c8c003146,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
965becd4-b0f7-4c4f-9ec4-c60c8c003146,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
965becd4-b0f7-4c4f-9ec4-c60c8c003146,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
965becd4-b0f7-4c4f-9ec4-c60c8c003146,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
965becd4-b0f7-4c4f-9ec4-c60c8c003146,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
965becd4-b0f7-4c4f-9ec4-c60c8c003146,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
965becd4-b0f7-4c4f-9ec4-c60c8c003146,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
965becd4-b0f7-4c4f-9ec4-c60c8c003146,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
965becd4-b0f7-4c4f-9ec4-c60c8c003146,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
965becd4-b0f7-4c4f-9ec4-c60c8c003146,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
965becd4-b0f7-4c4f-9ec4-c60c8c003146,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
965becd4-b0f7-4c4f-9ec4-c60c8c003146,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
965becd4-b0f7-4c4f-9ec4-c60c8c003146,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
6a702af6-2636-43bc-b324-49cfad7cb405,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
6a702af6-2636-43bc-b324-49cfad7cb405,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
6a702af6-2636-43bc-b324-49cfad7cb405,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
6a702af6-2636-43bc-b324-49cfad7cb405,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
6a702af6-2636-43bc-b324-49cfad7cb405,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
6a702af6-2636-43bc-b324-49cfad7cb405,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
6a702af6-2636-43bc-b324-49cfad7cb405,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
6a702af6-2636-43bc-b324-49cfad7cb405,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
6a702af6-2636-43bc-b324-49cfad7cb405,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
6a702af6-2636-43bc-b324-49cfad7cb405,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
6a702af6-2636-43bc-b324-49cfad7cb405,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
6a702af6-2636-43bc-b324-49cfad7cb405,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
6a702af6-2636-43bc-b324-49cfad7cb405,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
6a702af6-2636-43bc-b324-49cfad7cb405,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
6a702af6-2636-43bc-b324-49cfad7cb405,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
6a702af6-2636-43bc-b324-49cfad7cb405,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
6a702af6-2636-43bc-b324-49cfad7cb405,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
4b7a817a-cee7-44a4-bf39-027b4e6927f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Table 1.11: Second-degree block summary.,True,Second-Degree Atrioventricular Block,,,,
838b5f4d-5f59-42df-84a3-1147c2b2f546,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Third-Degree Atrioventricular Block,False,Third-Degree Atrioventricular Block,,,,
6a627e7a-e68d-4a4a-bc47-618a9f09673d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
6a627e7a-e68d-4a4a-bc47-618a9f09673d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
6a627e7a-e68d-4a4a-bc47-618a9f09673d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
6a627e7a-e68d-4a4a-bc47-618a9f09673d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
6a627e7a-e68d-4a4a-bc47-618a9f09673d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
6a627e7a-e68d-4a4a-bc47-618a9f09673d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
6a627e7a-e68d-4a4a-bc47-618a9f09673d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
6a627e7a-e68d-4a4a-bc47-618a9f09673d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
6a627e7a-e68d-4a4a-bc47-618a9f09673d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
6a627e7a-e68d-4a4a-bc47-618a9f09673d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
6a627e7a-e68d-4a4a-bc47-618a9f09673d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
6a627e7a-e68d-4a4a-bc47-618a9f09673d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
6a627e7a-e68d-4a4a-bc47-618a9f09673d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
6a627e7a-e68d-4a4a-bc47-618a9f09673d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
6a627e7a-e68d-4a4a-bc47-618a9f09673d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
6a627e7a-e68d-4a4a-bc47-618a9f09673d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
6a627e7a-e68d-4a4a-bc47-618a9f09673d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
5731ea50-aafe-424d-a1a4-4dbc21be5571,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Table 1.12: Third-degree block summary.,True,Third-Degree Atrioventricular Block,,,,
249b7a95-1aac-48e5-a38e-113f06cde5c1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Left Bundle Branch Block,False,Left Bundle Branch Block,,,,
a885ba4a-0060-4a68-b88b-691adcaf1c08,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"A left bundle branch block (LBBB) is generated when the conductivity of the His-Purkinje system in the left ventricle is compromised, either through damage or disease. The ECG changes, and criteria for LBBB relate to these changes in conductivity and the left-side location.",True,Left Bundle Branch Block,,,,
b9c43b31-4741-42d7-9062-f13fc595ebb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b9c43b31-4741-42d7-9062-f13fc595ebb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b9c43b31-4741-42d7-9062-f13fc595ebb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b9c43b31-4741-42d7-9062-f13fc595ebb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b9c43b31-4741-42d7-9062-f13fc595ebb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b9c43b31-4741-42d7-9062-f13fc595ebb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b9c43b31-4741-42d7-9062-f13fc595ebb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b9c43b31-4741-42d7-9062-f13fc595ebb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b9c43b31-4741-42d7-9062-f13fc595ebb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b9c43b31-4741-42d7-9062-f13fc595ebb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b9c43b31-4741-42d7-9062-f13fc595ebb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b9c43b31-4741-42d7-9062-f13fc595ebb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b9c43b31-4741-42d7-9062-f13fc595ebb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b9c43b31-4741-42d7-9062-f13fc595ebb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b9c43b31-4741-42d7-9062-f13fc595ebb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b9c43b31-4741-42d7-9062-f13fc595ebb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b9c43b31-4741-42d7-9062-f13fc595ebb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5003ffbe-c402-4787-8e7d-871808215857,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The lateral leads (I, V5, and V6) normally show a downward deflecting Q-wave as normal septal deflection initially occurs left-to-right (i.e., away from the lateral leads). In LBBB the change in direction to right-to-left, plus the longer duration, eliminates the Q-wave from the lateral leads, and Q-waves will be small in aVL.",True,Left Bundle Branch Block,,,,
386da169-3118-4890-acd0-090f9837d56a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
386da169-3118-4890-acd0-090f9837d56a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
386da169-3118-4890-acd0-090f9837d56a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
386da169-3118-4890-acd0-090f9837d56a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
386da169-3118-4890-acd0-090f9837d56a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
386da169-3118-4890-acd0-090f9837d56a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
386da169-3118-4890-acd0-090f9837d56a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
386da169-3118-4890-acd0-090f9837d56a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
386da169-3118-4890-acd0-090f9837d56a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
386da169-3118-4890-acd0-090f9837d56a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
386da169-3118-4890-acd0-090f9837d56a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
386da169-3118-4890-acd0-090f9837d56a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
386da169-3118-4890-acd0-090f9837d56a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
386da169-3118-4890-acd0-090f9837d56a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
386da169-3118-4890-acd0-090f9837d56a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
386da169-3118-4890-acd0-090f9837d56a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
386da169-3118-4890-acd0-090f9837d56a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
b426998e-b2f7-45f5-9384-358fbd07063c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b426998e-b2f7-45f5-9384-358fbd07063c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b426998e-b2f7-45f5-9384-358fbd07063c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b426998e-b2f7-45f5-9384-358fbd07063c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b426998e-b2f7-45f5-9384-358fbd07063c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b426998e-b2f7-45f5-9384-358fbd07063c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b426998e-b2f7-45f5-9384-358fbd07063c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b426998e-b2f7-45f5-9384-358fbd07063c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b426998e-b2f7-45f5-9384-358fbd07063c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b426998e-b2f7-45f5-9384-358fbd07063c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b426998e-b2f7-45f5-9384-358fbd07063c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b426998e-b2f7-45f5-9384-358fbd07063c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b426998e-b2f7-45f5-9384-358fbd07063c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b426998e-b2f7-45f5-9384-358fbd07063c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b426998e-b2f7-45f5-9384-358fbd07063c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b426998e-b2f7-45f5-9384-358fbd07063c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b426998e-b2f7-45f5-9384-358fbd07063c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
02465077-e9fe-44b6-af9e-7b2a3ccc300a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Table 1.13: LBBB summary.,True,Left Bundle Branch Block,,,,
ff45bf96-ff60-4dcf-901a-f5eae19f5b0c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Right Bundle Branch Block,False,Right Bundle Branch Block,,,,
0660942b-c431-4fef-bdff-2afadb63a65b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The causes and manifestations of a right bundle branch block (RBBB) bear some similarities to those described for LBBB, but of course this time its depolarization of the right ventricle is delayed. Causes of RBBB include ischemic heart disease again as well as other myocardial diseases, but pulmonary issues such as pulmonary embolism and cor pulmonale can be added to the list.",True,Right Bundle Branch Block,,,,
56ee0865-ca9c-4123-aed4-68af33d60767,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
56ee0865-ca9c-4123-aed4-68af33d60767,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
56ee0865-ca9c-4123-aed4-68af33d60767,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
56ee0865-ca9c-4123-aed4-68af33d60767,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
56ee0865-ca9c-4123-aed4-68af33d60767,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
56ee0865-ca9c-4123-aed4-68af33d60767,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
56ee0865-ca9c-4123-aed4-68af33d60767,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
56ee0865-ca9c-4123-aed4-68af33d60767,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
56ee0865-ca9c-4123-aed4-68af33d60767,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
56ee0865-ca9c-4123-aed4-68af33d60767,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
56ee0865-ca9c-4123-aed4-68af33d60767,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
56ee0865-ca9c-4123-aed4-68af33d60767,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
56ee0865-ca9c-4123-aed4-68af33d60767,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
56ee0865-ca9c-4123-aed4-68af33d60767,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
56ee0865-ca9c-4123-aed4-68af33d60767,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
56ee0865-ca9c-4123-aed4-68af33d60767,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
56ee0865-ca9c-4123-aed4-68af33d60767,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
d81878ee-9a7f-47f7-970b-06982f2b4611,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Table 1.14: RBBB summary.,True,Right Bundle Branch Block,,,,
9f8bd995-ea55-475d-84d1-79c275a7a09f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Wolff-Parkinson-White Syndrome,False,Wolff-Parkinson-White Syndrome,,,,
9e0d8e26-2159-4a02-ac40-1eefd48aebc9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Normally the only electrical connection between the atria and the ventricles is the AV node. Otherwise the fibrous skeleton of the heart electrically insulates the atria from the ventricles. In Wolff-Parkinson-White (WPW) syndrome, that insulation is incomplete, and an “accessory pathway” connects the electrical system of the atria directly to the ventricles. If you think of the AV node as a bridge over the fibrous wall with regulated access, the accessory pathway is like a pathological tunnel under it with no regulation.",True,Wolff-Parkinson-White Syndrome,,,,
8932b12e-8f7b-4f3e-99c0-eb10915aa28d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
8932b12e-8f7b-4f3e-99c0-eb10915aa28d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
8932b12e-8f7b-4f3e-99c0-eb10915aa28d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
8932b12e-8f7b-4f3e-99c0-eb10915aa28d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
8932b12e-8f7b-4f3e-99c0-eb10915aa28d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
8932b12e-8f7b-4f3e-99c0-eb10915aa28d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
8932b12e-8f7b-4f3e-99c0-eb10915aa28d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
8932b12e-8f7b-4f3e-99c0-eb10915aa28d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
8932b12e-8f7b-4f3e-99c0-eb10915aa28d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
8932b12e-8f7b-4f3e-99c0-eb10915aa28d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
8932b12e-8f7b-4f3e-99c0-eb10915aa28d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
8932b12e-8f7b-4f3e-99c0-eb10915aa28d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
8932b12e-8f7b-4f3e-99c0-eb10915aa28d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
8932b12e-8f7b-4f3e-99c0-eb10915aa28d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
8932b12e-8f7b-4f3e-99c0-eb10915aa28d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
8932b12e-8f7b-4f3e-99c0-eb10915aa28d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
8932b12e-8f7b-4f3e-99c0-eb10915aa28d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
72b53cc1-11ff-43c7-8ea0-5a6600307f89,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"WPW syndrome is often asymptomatic, and patients do not require immediate treatment. However, if atrial fibrillation occurs in a WPW patient, the accessory pathway can allow the atrial fibrillation waves through to the ventricle (with no AV nodal refractory period to prevent them). Consequently a high ventricular rate is seen, and the risk of ventricular fibrillation being established means immediate clinical attention is required.",True,Wolff-Parkinson-White Syndrome,,,,
b8e89c40-c3dc-466d-a6e7-29261678636e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Hyper- and Hypocalcemia,False,Hyper- and Hypocalcemia,,,,
4d79d39a-1cd7-4bb8-afbf-207f41bee354,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
4d79d39a-1cd7-4bb8-afbf-207f41bee354,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
4d79d39a-1cd7-4bb8-afbf-207f41bee354,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
4d79d39a-1cd7-4bb8-afbf-207f41bee354,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
4d79d39a-1cd7-4bb8-afbf-207f41bee354,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
4d79d39a-1cd7-4bb8-afbf-207f41bee354,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
4d79d39a-1cd7-4bb8-afbf-207f41bee354,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
4d79d39a-1cd7-4bb8-afbf-207f41bee354,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
4d79d39a-1cd7-4bb8-afbf-207f41bee354,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
4d79d39a-1cd7-4bb8-afbf-207f41bee354,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
4d79d39a-1cd7-4bb8-afbf-207f41bee354,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
4d79d39a-1cd7-4bb8-afbf-207f41bee354,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
4d79d39a-1cd7-4bb8-afbf-207f41bee354,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
4d79d39a-1cd7-4bb8-afbf-207f41bee354,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
4d79d39a-1cd7-4bb8-afbf-207f41bee354,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
4d79d39a-1cd7-4bb8-afbf-207f41bee354,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
4d79d39a-1cd7-4bb8-afbf-207f41bee354,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
a2f790a2-be72-4f1f-8c4d-73999421f019,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
a2f790a2-be72-4f1f-8c4d-73999421f019,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
a2f790a2-be72-4f1f-8c4d-73999421f019,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
a2f790a2-be72-4f1f-8c4d-73999421f019,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
a2f790a2-be72-4f1f-8c4d-73999421f019,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
a2f790a2-be72-4f1f-8c4d-73999421f019,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
a2f790a2-be72-4f1f-8c4d-73999421f019,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
a2f790a2-be72-4f1f-8c4d-73999421f019,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
a2f790a2-be72-4f1f-8c4d-73999421f019,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
a2f790a2-be72-4f1f-8c4d-73999421f019,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
a2f790a2-be72-4f1f-8c4d-73999421f019,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
a2f790a2-be72-4f1f-8c4d-73999421f019,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
a2f790a2-be72-4f1f-8c4d-73999421f019,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
a2f790a2-be72-4f1f-8c4d-73999421f019,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
a2f790a2-be72-4f1f-8c4d-73999421f019,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
a2f790a2-be72-4f1f-8c4d-73999421f019,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
a2f790a2-be72-4f1f-8c4d-73999421f019,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
06eda0d8-9d72-4b64-b723-c9c8a64a366e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Table 1.16: Hyper- and hypocalcemia summary.,True,Hyper- and Hypocalcemia,,,,
6c92b72b-98ff-4c75-9b18-412760b94a59,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Hyper- and Hypokalemia,False,Hyper- and Hypokalemia,,,,
db13adfd-a3fe-4c46-b333-d482c2ecc254,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"The pathophysiology is not as simple as changes in extracellular K+ changing the electrochemical gradient for K+. Because of potassium’s role in maintaining the resting membrane potential, shifts in extracellular potassium can also influence the activity of Na+ and Ca++ channels.",True,Hyper- and Hypokalemia,,,,
ddabe12d-15f4-4f56-b229-0e6e09c02a35,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ddabe12d-15f4-4f56-b229-0e6e09c02a35,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ddabe12d-15f4-4f56-b229-0e6e09c02a35,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ddabe12d-15f4-4f56-b229-0e6e09c02a35,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ddabe12d-15f4-4f56-b229-0e6e09c02a35,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ddabe12d-15f4-4f56-b229-0e6e09c02a35,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ddabe12d-15f4-4f56-b229-0e6e09c02a35,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ddabe12d-15f4-4f56-b229-0e6e09c02a35,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ddabe12d-15f4-4f56-b229-0e6e09c02a35,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ddabe12d-15f4-4f56-b229-0e6e09c02a35,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ddabe12d-15f4-4f56-b229-0e6e09c02a35,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ddabe12d-15f4-4f56-b229-0e6e09c02a35,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ddabe12d-15f4-4f56-b229-0e6e09c02a35,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ddabe12d-15f4-4f56-b229-0e6e09c02a35,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ddabe12d-15f4-4f56-b229-0e6e09c02a35,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ddabe12d-15f4-4f56-b229-0e6e09c02a35,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ddabe12d-15f4-4f56-b229-0e6e09c02a35,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
8880c0d4-4040-4ad0-8013-e8ca908d18c9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"As hypokalemia also inhibits Na+-K+ ATPase, Na+ accumulates inside the cell. This in turn leads to an accumulation of Ca++ because of a subsequent failure of the Na+-Ca++ exchanger. Extended presence of these two positive ions inside the myocyte prolongs the action potential and may manifest as an increased width and amplitude of the P-wave.",True,Hyper- and Hypokalemia,,,,
1db0033e-25b0-4148-9c43-ff0fd589e14b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"As hypokalemia worsens, the problems with K+ conductance and repolarization increase, and the myocardium becomes susceptible to early after-depolarization (EAD) arrhythmias.",True,Hyper- and Hypokalemia,,,,
f5a67668-bd56-4451-9c28-84a9fb1bccec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
f5a67668-bd56-4451-9c28-84a9fb1bccec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
f5a67668-bd56-4451-9c28-84a9fb1bccec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
f5a67668-bd56-4451-9c28-84a9fb1bccec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
f5a67668-bd56-4451-9c28-84a9fb1bccec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
f5a67668-bd56-4451-9c28-84a9fb1bccec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
f5a67668-bd56-4451-9c28-84a9fb1bccec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
f5a67668-bd56-4451-9c28-84a9fb1bccec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
f5a67668-bd56-4451-9c28-84a9fb1bccec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
f5a67668-bd56-4451-9c28-84a9fb1bccec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
f5a67668-bd56-4451-9c28-84a9fb1bccec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
f5a67668-bd56-4451-9c28-84a9fb1bccec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
f5a67668-bd56-4451-9c28-84a9fb1bccec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
f5a67668-bd56-4451-9c28-84a9fb1bccec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
f5a67668-bd56-4451-9c28-84a9fb1bccec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
f5a67668-bd56-4451-9c28-84a9fb1bccec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
f5a67668-bd56-4451-9c28-84a9fb1bccec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fb56e512-1149-4e12-8b47-1375ec19436b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fb56e512-1149-4e12-8b47-1375ec19436b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fb56e512-1149-4e12-8b47-1375ec19436b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fb56e512-1149-4e12-8b47-1375ec19436b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fb56e512-1149-4e12-8b47-1375ec19436b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fb56e512-1149-4e12-8b47-1375ec19436b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fb56e512-1149-4e12-8b47-1375ec19436b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fb56e512-1149-4e12-8b47-1375ec19436b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fb56e512-1149-4e12-8b47-1375ec19436b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fb56e512-1149-4e12-8b47-1375ec19436b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fb56e512-1149-4e12-8b47-1375ec19436b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fb56e512-1149-4e12-8b47-1375ec19436b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fb56e512-1149-4e12-8b47-1375ec19436b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fb56e512-1149-4e12-8b47-1375ec19436b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fb56e512-1149-4e12-8b47-1375ec19436b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fb56e512-1149-4e12-8b47-1375ec19436b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
fb56e512-1149-4e12-8b47-1375ec19436b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
d5d2bb46-729e-4a50-abdc-3e6dc4e3d1ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
d5d2bb46-729e-4a50-abdc-3e6dc4e3d1ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
d5d2bb46-729e-4a50-abdc-3e6dc4e3d1ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
d5d2bb46-729e-4a50-abdc-3e6dc4e3d1ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
d5d2bb46-729e-4a50-abdc-3e6dc4e3d1ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
d5d2bb46-729e-4a50-abdc-3e6dc4e3d1ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
d5d2bb46-729e-4a50-abdc-3e6dc4e3d1ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
d5d2bb46-729e-4a50-abdc-3e6dc4e3d1ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
d5d2bb46-729e-4a50-abdc-3e6dc4e3d1ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
d5d2bb46-729e-4a50-abdc-3e6dc4e3d1ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
d5d2bb46-729e-4a50-abdc-3e6dc4e3d1ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
d5d2bb46-729e-4a50-abdc-3e6dc4e3d1ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
d5d2bb46-729e-4a50-abdc-3e6dc4e3d1ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
d5d2bb46-729e-4a50-abdc-3e6dc4e3d1ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
d5d2bb46-729e-4a50-abdc-3e6dc4e3d1ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
d5d2bb46-729e-4a50-abdc-3e6dc4e3d1ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
d5d2bb46-729e-4a50-abdc-3e6dc4e3d1ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
05ad2d86-a4f0-49c6-ac4c-40a3aa20c307,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
05ad2d86-a4f0-49c6-ac4c-40a3aa20c307,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
05ad2d86-a4f0-49c6-ac4c-40a3aa20c307,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
05ad2d86-a4f0-49c6-ac4c-40a3aa20c307,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
05ad2d86-a4f0-49c6-ac4c-40a3aa20c307,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
05ad2d86-a4f0-49c6-ac4c-40a3aa20c307,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
05ad2d86-a4f0-49c6-ac4c-40a3aa20c307,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
05ad2d86-a4f0-49c6-ac4c-40a3aa20c307,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
05ad2d86-a4f0-49c6-ac4c-40a3aa20c307,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
05ad2d86-a4f0-49c6-ac4c-40a3aa20c307,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
05ad2d86-a4f0-49c6-ac4c-40a3aa20c307,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
05ad2d86-a4f0-49c6-ac4c-40a3aa20c307,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
05ad2d86-a4f0-49c6-ac4c-40a3aa20c307,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
05ad2d86-a4f0-49c6-ac4c-40a3aa20c307,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
05ad2d86-a4f0-49c6-ac4c-40a3aa20c307,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
05ad2d86-a4f0-49c6-ac4c-40a3aa20c307,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
05ad2d86-a4f0-49c6-ac4c-40a3aa20c307,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
e00a0fc4-4188-4fb7-a633-faf324d5b173,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Table 1.17: Hypo- and hyperkalemia summary.,True,Hyper- and Hypokalemia,,,,
f990576b-74d7-4c28-8791-2030930ce61f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"References, resources, and further reading",False,"References, resources, and further reading",,,,
61b82598-249d-4626-aff9-36a03a2a6d48,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,Text,False,Text,,,,
7bba81d2-ff2d-485c-bdd2-a6078095cfa2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Burns, Ed, and Robert Buttner. Hypercalcaemia. Lift in the Fast Lane, 2021. https://litfl.com/hypercalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
28b50094-2ed2-42bb-9d82-d70820917407,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Burns, Ed, and Robert Buttner. Hypocalcaemia. Life in the Fast Lane, 2021. https://litfl.com/hypocalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
a47ec5f7-22a0-4306-93bf-b4b578997add,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Buttner, Robert, and Ed Burns. Hyperkalaemia. Life in the Fast Lane. https://litfl.com/hyperkalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
1176c10c-44a3-44a6-bf84-a1e7a28864cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Buttner, Robert, and Ed Burns. Hypokalaemia. Life in the Fast Lane, 2021. https://litfl.com/hypokalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
99396aad-93c3-4cc2-8560-961efa730f89,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Chhabra, Lovely, Amandeep Goyal, and Michael D. Benham. Wolff Parkinson White Syndrome. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK554437/, CC BY 4.0.",True,Text,,,,
49779e80-62b7-4b53-8fd5-4a5bfbc188f2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Custer, Adam M., Varun S. Yelamanchili, and Sarah L. Lappin. Multifocal Atrial Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459152/, CC BY 4.0.",True,Text,,,,
c02f342f-1231-4086-9238-2174f2848770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Farzam, Khashayar, and John R. Richards. Premature Ventricular Contraction. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532991/, CC BY 4.0.",True,Text,,,,
3d0b751e-494b-47a4-9f17-4be1afe892c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Foth, Christopher, Manesh Kumar Gangwani, and Heidi Alvey. Ventricular Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532954/, CC BY 4.0.",True,Text,,,,
32fcfce1-9a15-47a9-bb3e-533fb0d74a11,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Hafeez, Yamama, and Shamai A. Grossman. Sinus Bradycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK493201/, CC BY 4.0.",True,Text,,,,
10e27b2e-3e81-44f9-a643-fb3c54278ace,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Harkness, Weston T., and Mary Hicks. Right Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK507872/, CC BY 4.0.",True,Text,,,,
f6826976-690d-4261-8484-96a3fabea9ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Heaton, Joseph, and Srikanth Yandrapalli. Premature Atrial Contractions. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK559204/, CC BY 4.0.",True,Text,,,,
fe9a5578-5fec-4f6b-b3c3-f2e3e353b986,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Kashou, Anthony H., Amandeep Goyal, Tran Nguyen, and Lovely Chhabra. Atrioventricular Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459147/, CC BY 4.0.",True,Text,,,,
5b94b3c2-9fc9-4979-96c0-27c56d270e1a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,“Learn the Heart.” Healio. https://www.healio.com/cardiology/learn-the-heart.,True,Text,,,,
259de092-08f2-433a-90dc-cc6e86f772a1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Ludhwani, Dipesh, Amandeep Goyal, and Mandar Jagtap. Ventricular Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK537120/, CC BY 4.0.",True,Text,,,,
24027397-65ee-4a5f-83b4-2201d4ed7f46,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Nesheiwat, Zeid, Amandeep Goyal, and Mandar Jagtap. Atrial Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK526072/, CC BY 4.0.",True,Text,,,,
608e8f06-8c28-474a-90ea-9ccd64ea77b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Pipilas, Daniel C., Bruce A. Koplan, and Leonard S. Lilly. “The Electrocardiogram.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 4. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
74ab5b8e-a833-4b8b-a041-afc8b597eac4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Rodriguez Ziccardi, Mary, Amandeep Goyal, and Christopher V. Maani. Atrial Flutter. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK540985/, CC BY 4.0.",True,Text,,,,
f52583e8-7e37-47af-8cc1-90550f9300e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-15,"Scherbak, Dmitriy, and Gregory J. Hicks. Left Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK482167/, CC BY 4.0.",True,Text,,,,
07cc0cb1-683b-4612-be00-966cae0a9de9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,USMLE,False,USMLE,,,,
f2c5f71f-c264-4a72-aeac-50a8da0e3481,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f2c5f71f-c264-4a72-aeac-50a8da0e3481,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f2c5f71f-c264-4a72-aeac-50a8da0e3481,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f2c5f71f-c264-4a72-aeac-50a8da0e3481,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f2c5f71f-c264-4a72-aeac-50a8da0e3481,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f2c5f71f-c264-4a72-aeac-50a8da0e3481,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f2c5f71f-c264-4a72-aeac-50a8da0e3481,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f2c5f71f-c264-4a72-aeac-50a8da0e3481,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f2c5f71f-c264-4a72-aeac-50a8da0e3481,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f2c5f71f-c264-4a72-aeac-50a8da0e3481,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f2c5f71f-c264-4a72-aeac-50a8da0e3481,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f2c5f71f-c264-4a72-aeac-50a8da0e3481,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f2c5f71f-c264-4a72-aeac-50a8da0e3481,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f2c5f71f-c264-4a72-aeac-50a8da0e3481,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f2c5f71f-c264-4a72-aeac-50a8da0e3481,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f2c5f71f-c264-4a72-aeac-50a8da0e3481,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f2c5f71f-c264-4a72-aeac-50a8da0e3481,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
3a9143c9-44f7-4f17-8c69-b38a4be9bd2a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,10q22,False,10q22,,,,
1a00264b-791e-4f4a-9f43-80db1c1ee1a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,q24,False,q24,,,,
bcc46425-7e7b-4fb4-9551-f9dee7f9897c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,fibrillatory,False,fibrillatory,,,,
16687a14-f1b7-41d4-94f6-222415301881,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
16687a14-f1b7-41d4-94f6-222415301881,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
16687a14-f1b7-41d4-94f6-222415301881,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
16687a14-f1b7-41d4-94f6-222415301881,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
16687a14-f1b7-41d4-94f6-222415301881,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
16687a14-f1b7-41d4-94f6-222415301881,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
16687a14-f1b7-41d4-94f6-222415301881,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
16687a14-f1b7-41d4-94f6-222415301881,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
16687a14-f1b7-41d4-94f6-222415301881,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
16687a14-f1b7-41d4-94f6-222415301881,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
16687a14-f1b7-41d4-94f6-222415301881,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
16687a14-f1b7-41d4-94f6-222415301881,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
16687a14-f1b7-41d4-94f6-222415301881,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
16687a14-f1b7-41d4-94f6-222415301881,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
16687a14-f1b7-41d4-94f6-222415301881,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
16687a14-f1b7-41d4-94f6-222415301881,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
16687a14-f1b7-41d4-94f6-222415301881,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d394ecdd-6721-4a5f-b029-b933b3e6c2f9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Table 1.1: Atrial fibrillation summary.,True,fibrillatory,,,,
6c5b3ec2-a219-4143-b235-725057e16392,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Atrial Flutter,False,Atrial Flutter,,,,
44c3d2e9-76b7-43c6-8370-2523c8f3819f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
44c3d2e9-76b7-43c6-8370-2523c8f3819f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
44c3d2e9-76b7-43c6-8370-2523c8f3819f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
44c3d2e9-76b7-43c6-8370-2523c8f3819f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
44c3d2e9-76b7-43c6-8370-2523c8f3819f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
44c3d2e9-76b7-43c6-8370-2523c8f3819f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
44c3d2e9-76b7-43c6-8370-2523c8f3819f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
44c3d2e9-76b7-43c6-8370-2523c8f3819f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
44c3d2e9-76b7-43c6-8370-2523c8f3819f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
44c3d2e9-76b7-43c6-8370-2523c8f3819f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
44c3d2e9-76b7-43c6-8370-2523c8f3819f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
44c3d2e9-76b7-43c6-8370-2523c8f3819f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
44c3d2e9-76b7-43c6-8370-2523c8f3819f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
44c3d2e9-76b7-43c6-8370-2523c8f3819f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
44c3d2e9-76b7-43c6-8370-2523c8f3819f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
44c3d2e9-76b7-43c6-8370-2523c8f3819f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
44c3d2e9-76b7-43c6-8370-2523c8f3819f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
4bd2fb50-32cf-453f-947e-0552163f21d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,macroreentrant,False,macroreentrant,,,,
4e6b1d9e-059a-47d9-9f10-80af7e46b5f9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,cavotricuspid,False,cavotricuspid,,,,
c56a6534-6ca6-413b-9537-ccb6dc0f4c88,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"As with atrial fibrillation, the AV node’s refractory period prevents most of the P-waves from progressing to the ventricle, but commonly the AV conduction will be 2-to-1, so with an atrial rate of 300 bpm the ventricular rate will be 150 bpm. Parasympathetic stimulation or changes in AV node refractoriness can modify how many P-waves pass into the ventricle, but the the resultant rhythm is “regularly irregular.” When the heart rate is elevated, then distinguishing flutter from fibrillation becomes challenging and slowing ventricular rate pharmaceutically (adenosine) helps the flutter waves reemerge for a definitive diagnosis to be made.",True,cavotricuspid,,,,
3bfd036c-874e-4164-8c00-f69bf8697329,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Table 1.2: Atrial flutter summary.,True,cavotricuspid,,,,
107a6f90-d4f6-40ce-a721-ab2b111cdaf9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Multifocal Atrial Tachycardia,False,Multifocal Atrial Tachycardia,,,,
c87383d8-3ee7-49d4-9ef6-6a509c36abc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c87383d8-3ee7-49d4-9ef6-6a509c36abc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c87383d8-3ee7-49d4-9ef6-6a509c36abc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c87383d8-3ee7-49d4-9ef6-6a509c36abc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c87383d8-3ee7-49d4-9ef6-6a509c36abc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c87383d8-3ee7-49d4-9ef6-6a509c36abc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c87383d8-3ee7-49d4-9ef6-6a509c36abc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c87383d8-3ee7-49d4-9ef6-6a509c36abc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c87383d8-3ee7-49d4-9ef6-6a509c36abc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c87383d8-3ee7-49d4-9ef6-6a509c36abc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c87383d8-3ee7-49d4-9ef6-6a509c36abc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c87383d8-3ee7-49d4-9ef6-6a509c36abc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c87383d8-3ee7-49d4-9ef6-6a509c36abc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c87383d8-3ee7-49d4-9ef6-6a509c36abc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c87383d8-3ee7-49d4-9ef6-6a509c36abc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c87383d8-3ee7-49d4-9ef6-6a509c36abc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c87383d8-3ee7-49d4-9ef6-6a509c36abc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
ef437be2-d00a-40b7-9873-1a23fce05cd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"MAT frequently occurs in the setting of severe lung disease and, more specifically, during an exacerbation of lung disease. This rhythm is benign, and once the underlying lung disease is treated, it should resolve.",True,Multifocal Atrial Tachycardia,,,,
497d6efb-edf8-48ee-807a-7a604f90c4ef,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Table 1.3: MAT summary.,True,Multifocal Atrial Tachycardia,,,,
c1087d06-72a7-40d8-992e-1b0e38b619fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Premature Atrial Contraction,False,Premature Atrial Contraction,,,,
c1d9ed0e-6429-423f-8ff8-e3af603ac92d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A premature atrial contraction (PAC) is generated by a depolarization instigated outside of the SA node. This produces an extra P-wave, and consequently a shortening from previous P-P intervals is seen. The aberrant P-wave also has a different morphology from a sinus P-wave because of its different anatomical origin.",True,Premature Atrial Contraction,,,,
d9159fe4-cb86-4b76-9339-75fbe7ffa7c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
d9159fe4-cb86-4b76-9339-75fbe7ffa7c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
d9159fe4-cb86-4b76-9339-75fbe7ffa7c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
d9159fe4-cb86-4b76-9339-75fbe7ffa7c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
d9159fe4-cb86-4b76-9339-75fbe7ffa7c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
d9159fe4-cb86-4b76-9339-75fbe7ffa7c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
d9159fe4-cb86-4b76-9339-75fbe7ffa7c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
d9159fe4-cb86-4b76-9339-75fbe7ffa7c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
d9159fe4-cb86-4b76-9339-75fbe7ffa7c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
d9159fe4-cb86-4b76-9339-75fbe7ffa7c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
d9159fe4-cb86-4b76-9339-75fbe7ffa7c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
d9159fe4-cb86-4b76-9339-75fbe7ffa7c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
d9159fe4-cb86-4b76-9339-75fbe7ffa7c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
d9159fe4-cb86-4b76-9339-75fbe7ffa7c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
d9159fe4-cb86-4b76-9339-75fbe7ffa7c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
d9159fe4-cb86-4b76-9339-75fbe7ffa7c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
d9159fe4-cb86-4b76-9339-75fbe7ffa7c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
161b677e-5d95-452c-9fdd-06bbe7873158,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"If a PAC occurs when the AV node has not yet recovered from its refractory period, the PAC will fail to conduct to the ventricles; meaning the PAC will not be followed by a QRS complex or the ectopic P-R interval will be prolonged. The ECG will show a premature, ectopic P-wave and then no QRS complex afterward. When this occurs along with bigeminy, the ECG can appear as if there is sinus bradycardia.",True,Premature Atrial Contraction,,,,
bb5b6ee5-fbfa-46b4-87d6-f71161b052cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Table 1.4: PAC summary.,True,Premature Atrial Contraction,,,,
15e20ee8-8d52-4324-b686-5b462e66178c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Sinus Bradycardia,False,Sinus Bradycardia,,,,
24216f12-7bb4-4c69-9fb8-f14b1379a21e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Sinus bradycardia denotes a sinus rhythm below 60 bpm. Otherwise the ECG waveform is normal on an ECG with an upright P-wave in lead II preceding every QRS complex. There are many intrinsic causes associated with the heart itself, as well as extrinsic causes, some of which are listed table 1.5. Sinus bradycardia is usually asymptomatic as rates of 40–50 bpm can maintain hemodynamic stability. Rates below this can produce symptoms of fatigue, dizziness, and dyspnea on exertion.",True,Sinus Bradycardia,,,,
2d847daf-ed32-4654-b00a-aa3b4087a961,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Table 1.5: Intrinsic and extrinsic causes associated with the heart.,True,Sinus Bradycardia,,,,
047efbc7-d4d9-460e-bd27-9963c40e0e2f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Table 1.6: Sinus bradycardia summary.,True,Sinus Bradycardia,,,,
280377ad-48e1-4295-9d31-c17690bd8d40,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Premature Ventricular Contractions,False,Premature Ventricular Contractions,,,,
954bd3ba-00b2-441a-bbdc-f5d2f35fdd72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
954bd3ba-00b2-441a-bbdc-f5d2f35fdd72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
954bd3ba-00b2-441a-bbdc-f5d2f35fdd72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
954bd3ba-00b2-441a-bbdc-f5d2f35fdd72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
954bd3ba-00b2-441a-bbdc-f5d2f35fdd72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
954bd3ba-00b2-441a-bbdc-f5d2f35fdd72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
954bd3ba-00b2-441a-bbdc-f5d2f35fdd72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
954bd3ba-00b2-441a-bbdc-f5d2f35fdd72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
954bd3ba-00b2-441a-bbdc-f5d2f35fdd72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
954bd3ba-00b2-441a-bbdc-f5d2f35fdd72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
954bd3ba-00b2-441a-bbdc-f5d2f35fdd72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
954bd3ba-00b2-441a-bbdc-f5d2f35fdd72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
954bd3ba-00b2-441a-bbdc-f5d2f35fdd72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
954bd3ba-00b2-441a-bbdc-f5d2f35fdd72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
954bd3ba-00b2-441a-bbdc-f5d2f35fdd72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
954bd3ba-00b2-441a-bbdc-f5d2f35fdd72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
954bd3ba-00b2-441a-bbdc-f5d2f35fdd72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
6cd76757-cf40-4bdc-819d-095106ff4c74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Table 1.7: PVC summary.,True,Premature Ventricular Contractions,,,,
14ec1b4d-23c0-4ac3-91e3-9b59fa08cf32,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Ventricular Tachycardia,False,Ventricular Tachycardia,,,,
00b2ea87-7dd3-4955-a269-fcf5f2b8e9f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Ventricular tachycardia (VT) is caused by reentry currents being established in the ventricular myocardium or groups of ventricular myocytes that have aberrant electrical behavior. As such, VT is usually caused by underlying cardiac disease.",True,Ventricular Tachycardia,,,,
74855a41-f135-490c-aeb3-243a7d5cc15b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Like a PVC, the aberrant depolarizations do not follow the normal conduction pathways so are wide (>120 msecs), but unlike a PVC, VT involves a ventricular rate >100 bpm. With disorganized contractility and reduced filling time, VT can lead to hemodynamic instability and severe hypotension—hence it is life threatening.",True,Ventricular Tachycardia,,,,
3ae89690-22ef-4ce4-b837-261b8cb0b007,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The QRS morphology in VT is highly variable between patients and depends on where the arrhythmia originates. Consequently there are several ways to classify VT based on duration, symptoms, QRS morphology, rate, and origin.",True,Ventricular Tachycardia,,,,
7943263b-7f1f-4659-895e-b79a6752dede,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Sustained VT is any VT that lasts for more than 30 seconds or is symptomatic. Nonsustained VT lasts for less than 30 seconds and is asymptomatic.,True,Ventricular Tachycardia,,,,
ec541a92-396c-40dc-af91-ab16e264e2a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ec541a92-396c-40dc-af91-ab16e264e2a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ec541a92-396c-40dc-af91-ab16e264e2a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ec541a92-396c-40dc-af91-ab16e264e2a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ec541a92-396c-40dc-af91-ab16e264e2a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ec541a92-396c-40dc-af91-ab16e264e2a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ec541a92-396c-40dc-af91-ab16e264e2a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ec541a92-396c-40dc-af91-ab16e264e2a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ec541a92-396c-40dc-af91-ab16e264e2a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ec541a92-396c-40dc-af91-ab16e264e2a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ec541a92-396c-40dc-af91-ab16e264e2a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ec541a92-396c-40dc-af91-ab16e264e2a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ec541a92-396c-40dc-af91-ab16e264e2a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ec541a92-396c-40dc-af91-ab16e264e2a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ec541a92-396c-40dc-af91-ab16e264e2a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ec541a92-396c-40dc-af91-ab16e264e2a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ec541a92-396c-40dc-af91-ab16e264e2a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
a6fffc6c-d6db-4956-baea-946f16af5157,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a6fffc6c-d6db-4956-baea-946f16af5157,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a6fffc6c-d6db-4956-baea-946f16af5157,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a6fffc6c-d6db-4956-baea-946f16af5157,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a6fffc6c-d6db-4956-baea-946f16af5157,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a6fffc6c-d6db-4956-baea-946f16af5157,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a6fffc6c-d6db-4956-baea-946f16af5157,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a6fffc6c-d6db-4956-baea-946f16af5157,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a6fffc6c-d6db-4956-baea-946f16af5157,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a6fffc6c-d6db-4956-baea-946f16af5157,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a6fffc6c-d6db-4956-baea-946f16af5157,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a6fffc6c-d6db-4956-baea-946f16af5157,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a6fffc6c-d6db-4956-baea-946f16af5157,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a6fffc6c-d6db-4956-baea-946f16af5157,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a6fffc6c-d6db-4956-baea-946f16af5157,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a6fffc6c-d6db-4956-baea-946f16af5157,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a6fffc6c-d6db-4956-baea-946f16af5157,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
56f792c9-0588-4730-a641-efcbefadf175,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Torsades de pointes is associated with a prolonged QT interval (>600 msecs) that helps distinguish it from other forms of polymorphous VT. The longer QT interval can be caused by ionic abnormalities that reduce the repolarizing current of Phase 3 of the cardiac action potential. This makes the myocardium susceptible to early after-depolarizations—the trigger for torsades de pointes. These after-depolarizations do not happen uniformly across the myocardium and are more common in endocardial tissue where the repolarization currents are slower. So torsades de pointes arises from the after-depolarizations causing reentry currents in neighboring tissue.,True,Ventricular Tachycardia,,,,
557c97de-e289-404b-94ed-d463174cab71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Both common garden variety VTs and torsades de pointes can progress to ventricular fibrillation.,True,Ventricular Tachycardia,,,,
41c86d3d-6ece-4cd6-9cf7-d02c05c7a680,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Table 1.8: VT summary.,True,Ventricular Tachycardia,,,,
0891bcdc-4b0b-4855-9efe-f05de1780659,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Ventricular Fibrillation,False,Ventricular Fibrillation,,,,
15ca0637-0d75-4f11-8fb0-0a7159e2f7ff,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Ventricular fibrillation (VF) occurs when the ventricular rate exceeds 400 bpm. The disorganized and uncoordinated contraction of the myocardium causes cardiac output to fall to catastrophic levels. Rates of survival for out-of-hospital VF are low.,True,Ventricular Fibrillation,,,,
094b68c6-bd1c-4f2d-bae3-520ab35099c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
094b68c6-bd1c-4f2d-bae3-520ab35099c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
094b68c6-bd1c-4f2d-bae3-520ab35099c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
094b68c6-bd1c-4f2d-bae3-520ab35099c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
094b68c6-bd1c-4f2d-bae3-520ab35099c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
094b68c6-bd1c-4f2d-bae3-520ab35099c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
094b68c6-bd1c-4f2d-bae3-520ab35099c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
094b68c6-bd1c-4f2d-bae3-520ab35099c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
094b68c6-bd1c-4f2d-bae3-520ab35099c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
094b68c6-bd1c-4f2d-bae3-520ab35099c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
094b68c6-bd1c-4f2d-bae3-520ab35099c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
094b68c6-bd1c-4f2d-bae3-520ab35099c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
094b68c6-bd1c-4f2d-bae3-520ab35099c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
094b68c6-bd1c-4f2d-bae3-520ab35099c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
094b68c6-bd1c-4f2d-bae3-520ab35099c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
094b68c6-bd1c-4f2d-bae3-520ab35099c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
094b68c6-bd1c-4f2d-bae3-520ab35099c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
2d901688-030e-4650-b383-0dfcd6d097b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Table 1.9: VF summary.,True,Ventricular Fibrillation,,,,
44013d27-456a-49e4-a1ca-066ec4f6cc18,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,First-Degree Atrioventricular Block,False,First-Degree Atrioventricular Block,,,,
39e75f6e-f264-4902-96a5-77678afdaac9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
39e75f6e-f264-4902-96a5-77678afdaac9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
39e75f6e-f264-4902-96a5-77678afdaac9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
39e75f6e-f264-4902-96a5-77678afdaac9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
39e75f6e-f264-4902-96a5-77678afdaac9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
39e75f6e-f264-4902-96a5-77678afdaac9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
39e75f6e-f264-4902-96a5-77678afdaac9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
39e75f6e-f264-4902-96a5-77678afdaac9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
39e75f6e-f264-4902-96a5-77678afdaac9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
39e75f6e-f264-4902-96a5-77678afdaac9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
39e75f6e-f264-4902-96a5-77678afdaac9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
39e75f6e-f264-4902-96a5-77678afdaac9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
39e75f6e-f264-4902-96a5-77678afdaac9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
39e75f6e-f264-4902-96a5-77678afdaac9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
39e75f6e-f264-4902-96a5-77678afdaac9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
39e75f6e-f264-4902-96a5-77678afdaac9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
39e75f6e-f264-4902-96a5-77678afdaac9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ccae530d-204b-4e76-b694-514ae30351e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ccae530d-204b-4e76-b694-514ae30351e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ccae530d-204b-4e76-b694-514ae30351e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ccae530d-204b-4e76-b694-514ae30351e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ccae530d-204b-4e76-b694-514ae30351e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ccae530d-204b-4e76-b694-514ae30351e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ccae530d-204b-4e76-b694-514ae30351e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ccae530d-204b-4e76-b694-514ae30351e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ccae530d-204b-4e76-b694-514ae30351e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ccae530d-204b-4e76-b694-514ae30351e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ccae530d-204b-4e76-b694-514ae30351e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ccae530d-204b-4e76-b694-514ae30351e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ccae530d-204b-4e76-b694-514ae30351e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ccae530d-204b-4e76-b694-514ae30351e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ccae530d-204b-4e76-b694-514ae30351e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ccae530d-204b-4e76-b694-514ae30351e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ccae530d-204b-4e76-b694-514ae30351e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
160e0aee-c60e-41fb-8124-6dfb8f0b01ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Table 1.10: First-degree block summary.,True,First-Degree Atrioventricular Block,,,,
280a54db-a26c-4dcb-9932-c8fc99a5b86f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Second-Degree Atrioventricular Block,False,Second-Degree Atrioventricular Block,,,,
5b6212c6-359d-4677-aaeb-d71a84ab5290,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A second-degree atrioventricular block also has changes in P-R interval, but it starts to show failure of the P-wave to propagate a QRS complex every time (i.e., intermittently the depolarization fails to reach the ventricles). The pattern of missed ventricular depolarizations, or blocked P-waves, is often very regular and described as a ratio of P-waves to QRS complex. The way in which the P-R interval changes in relation to the blocked P-waves produces subclassifications of second-degree blocks, Mobitz I and II.",True,Second-Degree Atrioventricular Block,,,,
921b9f59-e70b-4120-a15e-6395659eb524,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
921b9f59-e70b-4120-a15e-6395659eb524,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
921b9f59-e70b-4120-a15e-6395659eb524,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
921b9f59-e70b-4120-a15e-6395659eb524,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
921b9f59-e70b-4120-a15e-6395659eb524,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
921b9f59-e70b-4120-a15e-6395659eb524,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
921b9f59-e70b-4120-a15e-6395659eb524,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
921b9f59-e70b-4120-a15e-6395659eb524,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
921b9f59-e70b-4120-a15e-6395659eb524,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
921b9f59-e70b-4120-a15e-6395659eb524,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
921b9f59-e70b-4120-a15e-6395659eb524,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
921b9f59-e70b-4120-a15e-6395659eb524,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
921b9f59-e70b-4120-a15e-6395659eb524,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
921b9f59-e70b-4120-a15e-6395659eb524,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
921b9f59-e70b-4120-a15e-6395659eb524,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
921b9f59-e70b-4120-a15e-6395659eb524,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
921b9f59-e70b-4120-a15e-6395659eb524,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
540c9614-0f01-4202-b8c4-f3666d44ce80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
540c9614-0f01-4202-b8c4-f3666d44ce80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
540c9614-0f01-4202-b8c4-f3666d44ce80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
540c9614-0f01-4202-b8c4-f3666d44ce80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
540c9614-0f01-4202-b8c4-f3666d44ce80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
540c9614-0f01-4202-b8c4-f3666d44ce80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
540c9614-0f01-4202-b8c4-f3666d44ce80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
540c9614-0f01-4202-b8c4-f3666d44ce80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
540c9614-0f01-4202-b8c4-f3666d44ce80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
540c9614-0f01-4202-b8c4-f3666d44ce80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
540c9614-0f01-4202-b8c4-f3666d44ce80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
540c9614-0f01-4202-b8c4-f3666d44ce80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
540c9614-0f01-4202-b8c4-f3666d44ce80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
540c9614-0f01-4202-b8c4-f3666d44ce80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
540c9614-0f01-4202-b8c4-f3666d44ce80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
540c9614-0f01-4202-b8c4-f3666d44ce80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
540c9614-0f01-4202-b8c4-f3666d44ce80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
7f295285-1a55-4a80-99b5-fed8c116b492,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Table 1.11: Second-degree block summary.,True,Second-Degree Atrioventricular Block,,,,
b3f5301b-51c2-49f9-bd31-e44d1b0c7a0b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Third-Degree Atrioventricular Block,False,Third-Degree Atrioventricular Block,,,,
96b74e82-0f70-4025-b536-86c2dfa7a1fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
96b74e82-0f70-4025-b536-86c2dfa7a1fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
96b74e82-0f70-4025-b536-86c2dfa7a1fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
96b74e82-0f70-4025-b536-86c2dfa7a1fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
96b74e82-0f70-4025-b536-86c2dfa7a1fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
96b74e82-0f70-4025-b536-86c2dfa7a1fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
96b74e82-0f70-4025-b536-86c2dfa7a1fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
96b74e82-0f70-4025-b536-86c2dfa7a1fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
96b74e82-0f70-4025-b536-86c2dfa7a1fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
96b74e82-0f70-4025-b536-86c2dfa7a1fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
96b74e82-0f70-4025-b536-86c2dfa7a1fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
96b74e82-0f70-4025-b536-86c2dfa7a1fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
96b74e82-0f70-4025-b536-86c2dfa7a1fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
96b74e82-0f70-4025-b536-86c2dfa7a1fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
96b74e82-0f70-4025-b536-86c2dfa7a1fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
96b74e82-0f70-4025-b536-86c2dfa7a1fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
96b74e82-0f70-4025-b536-86c2dfa7a1fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
c987e2fe-2f82-4db4-8f58-28a776d7d262,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Table 1.12: Third-degree block summary.,True,Third-Degree Atrioventricular Block,,,,
c18a80a5-c43e-4407-8d2c-0b19493c4bf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Left Bundle Branch Block,False,Left Bundle Branch Block,,,,
404d5982-fd6f-43ad-96fc-3d0fd3210f4f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"A left bundle branch block (LBBB) is generated when the conductivity of the His-Purkinje system in the left ventricle is compromised, either through damage or disease. The ECG changes, and criteria for LBBB relate to these changes in conductivity and the left-side location.",True,Left Bundle Branch Block,,,,
b0434d0b-7ad8-491b-a4ca-a4f01327d683,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b0434d0b-7ad8-491b-a4ca-a4f01327d683,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b0434d0b-7ad8-491b-a4ca-a4f01327d683,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b0434d0b-7ad8-491b-a4ca-a4f01327d683,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b0434d0b-7ad8-491b-a4ca-a4f01327d683,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b0434d0b-7ad8-491b-a4ca-a4f01327d683,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b0434d0b-7ad8-491b-a4ca-a4f01327d683,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b0434d0b-7ad8-491b-a4ca-a4f01327d683,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b0434d0b-7ad8-491b-a4ca-a4f01327d683,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b0434d0b-7ad8-491b-a4ca-a4f01327d683,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b0434d0b-7ad8-491b-a4ca-a4f01327d683,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b0434d0b-7ad8-491b-a4ca-a4f01327d683,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b0434d0b-7ad8-491b-a4ca-a4f01327d683,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b0434d0b-7ad8-491b-a4ca-a4f01327d683,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b0434d0b-7ad8-491b-a4ca-a4f01327d683,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b0434d0b-7ad8-491b-a4ca-a4f01327d683,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b0434d0b-7ad8-491b-a4ca-a4f01327d683,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
85a3a551-fb41-41e6-abe7-b10bda366f1b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The lateral leads (I, V5, and V6) normally show a downward deflecting Q-wave as normal septal deflection initially occurs left-to-right (i.e., away from the lateral leads). In LBBB the change in direction to right-to-left, plus the longer duration, eliminates the Q-wave from the lateral leads, and Q-waves will be small in aVL.",True,Left Bundle Branch Block,,,,
3b313021-df4f-40cb-8c03-c0b3f345c596,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
3b313021-df4f-40cb-8c03-c0b3f345c596,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
3b313021-df4f-40cb-8c03-c0b3f345c596,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
3b313021-df4f-40cb-8c03-c0b3f345c596,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
3b313021-df4f-40cb-8c03-c0b3f345c596,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
3b313021-df4f-40cb-8c03-c0b3f345c596,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
3b313021-df4f-40cb-8c03-c0b3f345c596,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
3b313021-df4f-40cb-8c03-c0b3f345c596,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
3b313021-df4f-40cb-8c03-c0b3f345c596,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
3b313021-df4f-40cb-8c03-c0b3f345c596,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
3b313021-df4f-40cb-8c03-c0b3f345c596,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
3b313021-df4f-40cb-8c03-c0b3f345c596,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
3b313021-df4f-40cb-8c03-c0b3f345c596,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
3b313021-df4f-40cb-8c03-c0b3f345c596,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
3b313021-df4f-40cb-8c03-c0b3f345c596,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
3b313021-df4f-40cb-8c03-c0b3f345c596,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
3b313021-df4f-40cb-8c03-c0b3f345c596,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f4abaff4-f326-42b5-8f5e-31d686f273e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
f4abaff4-f326-42b5-8f5e-31d686f273e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
f4abaff4-f326-42b5-8f5e-31d686f273e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
f4abaff4-f326-42b5-8f5e-31d686f273e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
f4abaff4-f326-42b5-8f5e-31d686f273e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
f4abaff4-f326-42b5-8f5e-31d686f273e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
f4abaff4-f326-42b5-8f5e-31d686f273e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
f4abaff4-f326-42b5-8f5e-31d686f273e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
f4abaff4-f326-42b5-8f5e-31d686f273e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
f4abaff4-f326-42b5-8f5e-31d686f273e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
f4abaff4-f326-42b5-8f5e-31d686f273e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
f4abaff4-f326-42b5-8f5e-31d686f273e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
f4abaff4-f326-42b5-8f5e-31d686f273e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
f4abaff4-f326-42b5-8f5e-31d686f273e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
f4abaff4-f326-42b5-8f5e-31d686f273e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
f4abaff4-f326-42b5-8f5e-31d686f273e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
f4abaff4-f326-42b5-8f5e-31d686f273e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
06c2a3bb-e99b-4e5f-aae3-19f57ea8cc67,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Table 1.13: LBBB summary.,True,Left Bundle Branch Block,,,,
35cc519a-c639-4206-a551-c819ebe62fad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Right Bundle Branch Block,False,Right Bundle Branch Block,,,,
a4c04337-d90e-4589-9008-f1b68338e75f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The causes and manifestations of a right bundle branch block (RBBB) bear some similarities to those described for LBBB, but of course this time its depolarization of the right ventricle is delayed. Causes of RBBB include ischemic heart disease again as well as other myocardial diseases, but pulmonary issues such as pulmonary embolism and cor pulmonale can be added to the list.",True,Right Bundle Branch Block,,,,
7cd307c0-7673-4219-a43b-b2a80177fc8c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
7cd307c0-7673-4219-a43b-b2a80177fc8c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
7cd307c0-7673-4219-a43b-b2a80177fc8c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
7cd307c0-7673-4219-a43b-b2a80177fc8c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
7cd307c0-7673-4219-a43b-b2a80177fc8c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
7cd307c0-7673-4219-a43b-b2a80177fc8c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
7cd307c0-7673-4219-a43b-b2a80177fc8c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
7cd307c0-7673-4219-a43b-b2a80177fc8c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
7cd307c0-7673-4219-a43b-b2a80177fc8c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
7cd307c0-7673-4219-a43b-b2a80177fc8c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
7cd307c0-7673-4219-a43b-b2a80177fc8c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
7cd307c0-7673-4219-a43b-b2a80177fc8c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
7cd307c0-7673-4219-a43b-b2a80177fc8c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
7cd307c0-7673-4219-a43b-b2a80177fc8c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
7cd307c0-7673-4219-a43b-b2a80177fc8c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
7cd307c0-7673-4219-a43b-b2a80177fc8c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
7cd307c0-7673-4219-a43b-b2a80177fc8c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
ace20f8f-386e-49fb-b452-4f430dd3b142,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Table 1.14: RBBB summary.,True,Right Bundle Branch Block,,,,
8dc6b6c9-e89c-4440-b25e-5bce44ab159f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Wolff-Parkinson-White Syndrome,False,Wolff-Parkinson-White Syndrome,,,,
c79ce460-a5d6-4426-bc19-38172f174fd4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Normally the only electrical connection between the atria and the ventricles is the AV node. Otherwise the fibrous skeleton of the heart electrically insulates the atria from the ventricles. In Wolff-Parkinson-White (WPW) syndrome, that insulation is incomplete, and an “accessory pathway” connects the electrical system of the atria directly to the ventricles. If you think of the AV node as a bridge over the fibrous wall with regulated access, the accessory pathway is like a pathological tunnel under it with no regulation.",True,Wolff-Parkinson-White Syndrome,,,,
965b00fe-d63c-4de3-b8f6-9abc1e03598f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
965b00fe-d63c-4de3-b8f6-9abc1e03598f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
965b00fe-d63c-4de3-b8f6-9abc1e03598f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
965b00fe-d63c-4de3-b8f6-9abc1e03598f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
965b00fe-d63c-4de3-b8f6-9abc1e03598f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
965b00fe-d63c-4de3-b8f6-9abc1e03598f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
965b00fe-d63c-4de3-b8f6-9abc1e03598f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
965b00fe-d63c-4de3-b8f6-9abc1e03598f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
965b00fe-d63c-4de3-b8f6-9abc1e03598f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
965b00fe-d63c-4de3-b8f6-9abc1e03598f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
965b00fe-d63c-4de3-b8f6-9abc1e03598f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
965b00fe-d63c-4de3-b8f6-9abc1e03598f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
965b00fe-d63c-4de3-b8f6-9abc1e03598f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
965b00fe-d63c-4de3-b8f6-9abc1e03598f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
965b00fe-d63c-4de3-b8f6-9abc1e03598f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
965b00fe-d63c-4de3-b8f6-9abc1e03598f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
965b00fe-d63c-4de3-b8f6-9abc1e03598f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
001a0c90-60e2-404c-9d34-d127a1b50ef7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"WPW syndrome is often asymptomatic, and patients do not require immediate treatment. However, if atrial fibrillation occurs in a WPW patient, the accessory pathway can allow the atrial fibrillation waves through to the ventricle (with no AV nodal refractory period to prevent them). Consequently a high ventricular rate is seen, and the risk of ventricular fibrillation being established means immediate clinical attention is required.",True,Wolff-Parkinson-White Syndrome,,,,
bd1d7e85-5fdc-430d-adf0-1d7f20158aad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Hyper- and Hypocalcemia,False,Hyper- and Hypocalcemia,,,,
3f3a44f8-7041-42b1-b70a-a4a67eb5ffcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3f3a44f8-7041-42b1-b70a-a4a67eb5ffcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3f3a44f8-7041-42b1-b70a-a4a67eb5ffcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3f3a44f8-7041-42b1-b70a-a4a67eb5ffcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3f3a44f8-7041-42b1-b70a-a4a67eb5ffcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3f3a44f8-7041-42b1-b70a-a4a67eb5ffcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3f3a44f8-7041-42b1-b70a-a4a67eb5ffcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3f3a44f8-7041-42b1-b70a-a4a67eb5ffcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3f3a44f8-7041-42b1-b70a-a4a67eb5ffcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3f3a44f8-7041-42b1-b70a-a4a67eb5ffcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3f3a44f8-7041-42b1-b70a-a4a67eb5ffcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3f3a44f8-7041-42b1-b70a-a4a67eb5ffcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3f3a44f8-7041-42b1-b70a-a4a67eb5ffcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3f3a44f8-7041-42b1-b70a-a4a67eb5ffcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3f3a44f8-7041-42b1-b70a-a4a67eb5ffcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3f3a44f8-7041-42b1-b70a-a4a67eb5ffcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3f3a44f8-7041-42b1-b70a-a4a67eb5ffcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
284b72e5-04dd-4fb5-bb2a-cd59373b9eea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
284b72e5-04dd-4fb5-bb2a-cd59373b9eea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
284b72e5-04dd-4fb5-bb2a-cd59373b9eea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
284b72e5-04dd-4fb5-bb2a-cd59373b9eea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
284b72e5-04dd-4fb5-bb2a-cd59373b9eea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
284b72e5-04dd-4fb5-bb2a-cd59373b9eea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
284b72e5-04dd-4fb5-bb2a-cd59373b9eea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
284b72e5-04dd-4fb5-bb2a-cd59373b9eea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
284b72e5-04dd-4fb5-bb2a-cd59373b9eea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
284b72e5-04dd-4fb5-bb2a-cd59373b9eea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
284b72e5-04dd-4fb5-bb2a-cd59373b9eea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
284b72e5-04dd-4fb5-bb2a-cd59373b9eea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
284b72e5-04dd-4fb5-bb2a-cd59373b9eea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
284b72e5-04dd-4fb5-bb2a-cd59373b9eea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
284b72e5-04dd-4fb5-bb2a-cd59373b9eea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
284b72e5-04dd-4fb5-bb2a-cd59373b9eea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
284b72e5-04dd-4fb5-bb2a-cd59373b9eea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
af0e551d-236c-4496-b6c1-416378c59ddd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Table 1.16: Hyper- and hypocalcemia summary.,True,Hyper- and Hypocalcemia,,,,
841419ad-88c3-4967-848c-0848e4843dde,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Hyper- and Hypokalemia,False,Hyper- and Hypokalemia,,,,
b2b36105-419c-4f96-8cfa-bc7be5331354,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"The pathophysiology is not as simple as changes in extracellular K+ changing the electrochemical gradient for K+. Because of potassium’s role in maintaining the resting membrane potential, shifts in extracellular potassium can also influence the activity of Na+ and Ca++ channels.",True,Hyper- and Hypokalemia,,,,
22b88473-0b36-4fe8-b128-345557c784fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
22b88473-0b36-4fe8-b128-345557c784fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
22b88473-0b36-4fe8-b128-345557c784fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
22b88473-0b36-4fe8-b128-345557c784fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
22b88473-0b36-4fe8-b128-345557c784fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
22b88473-0b36-4fe8-b128-345557c784fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
22b88473-0b36-4fe8-b128-345557c784fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
22b88473-0b36-4fe8-b128-345557c784fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
22b88473-0b36-4fe8-b128-345557c784fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
22b88473-0b36-4fe8-b128-345557c784fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
22b88473-0b36-4fe8-b128-345557c784fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
22b88473-0b36-4fe8-b128-345557c784fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
22b88473-0b36-4fe8-b128-345557c784fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
22b88473-0b36-4fe8-b128-345557c784fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
22b88473-0b36-4fe8-b128-345557c784fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
22b88473-0b36-4fe8-b128-345557c784fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
22b88473-0b36-4fe8-b128-345557c784fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
169f3146-89ce-41db-aeb5-17a08e741887,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"As hypokalemia also inhibits Na+-K+ ATPase, Na+ accumulates inside the cell. This in turn leads to an accumulation of Ca++ because of a subsequent failure of the Na+-Ca++ exchanger. Extended presence of these two positive ions inside the myocyte prolongs the action potential and may manifest as an increased width and amplitude of the P-wave.",True,Hyper- and Hypokalemia,,,,
14fcd856-5c9a-41e6-bc29-fd6c8cc521e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"As hypokalemia worsens, the problems with K+ conductance and repolarization increase, and the myocardium becomes susceptible to early after-depolarization (EAD) arrhythmias.",True,Hyper- and Hypokalemia,,,,
655f1c21-cc04-4c7e-8a43-ec3300727103,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
655f1c21-cc04-4c7e-8a43-ec3300727103,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
655f1c21-cc04-4c7e-8a43-ec3300727103,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
655f1c21-cc04-4c7e-8a43-ec3300727103,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
655f1c21-cc04-4c7e-8a43-ec3300727103,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
655f1c21-cc04-4c7e-8a43-ec3300727103,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
655f1c21-cc04-4c7e-8a43-ec3300727103,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
655f1c21-cc04-4c7e-8a43-ec3300727103,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
655f1c21-cc04-4c7e-8a43-ec3300727103,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
655f1c21-cc04-4c7e-8a43-ec3300727103,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
655f1c21-cc04-4c7e-8a43-ec3300727103,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
655f1c21-cc04-4c7e-8a43-ec3300727103,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
655f1c21-cc04-4c7e-8a43-ec3300727103,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
655f1c21-cc04-4c7e-8a43-ec3300727103,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
655f1c21-cc04-4c7e-8a43-ec3300727103,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
655f1c21-cc04-4c7e-8a43-ec3300727103,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
655f1c21-cc04-4c7e-8a43-ec3300727103,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
0a3c7337-68f5-4980-948e-eeab4f61b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3c7337-68f5-4980-948e-eeab4f61b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3c7337-68f5-4980-948e-eeab4f61b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3c7337-68f5-4980-948e-eeab4f61b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3c7337-68f5-4980-948e-eeab4f61b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3c7337-68f5-4980-948e-eeab4f61b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3c7337-68f5-4980-948e-eeab4f61b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3c7337-68f5-4980-948e-eeab4f61b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3c7337-68f5-4980-948e-eeab4f61b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3c7337-68f5-4980-948e-eeab4f61b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3c7337-68f5-4980-948e-eeab4f61b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3c7337-68f5-4980-948e-eeab4f61b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3c7337-68f5-4980-948e-eeab4f61b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3c7337-68f5-4980-948e-eeab4f61b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3c7337-68f5-4980-948e-eeab4f61b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3c7337-68f5-4980-948e-eeab4f61b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3c7337-68f5-4980-948e-eeab4f61b667,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
1ee40128-3db7-4eac-b324-8c403e5546a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
1ee40128-3db7-4eac-b324-8c403e5546a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
1ee40128-3db7-4eac-b324-8c403e5546a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
1ee40128-3db7-4eac-b324-8c403e5546a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
1ee40128-3db7-4eac-b324-8c403e5546a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
1ee40128-3db7-4eac-b324-8c403e5546a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
1ee40128-3db7-4eac-b324-8c403e5546a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
1ee40128-3db7-4eac-b324-8c403e5546a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
1ee40128-3db7-4eac-b324-8c403e5546a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
1ee40128-3db7-4eac-b324-8c403e5546a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
1ee40128-3db7-4eac-b324-8c403e5546a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
1ee40128-3db7-4eac-b324-8c403e5546a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
1ee40128-3db7-4eac-b324-8c403e5546a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
1ee40128-3db7-4eac-b324-8c403e5546a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
1ee40128-3db7-4eac-b324-8c403e5546a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
1ee40128-3db7-4eac-b324-8c403e5546a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
1ee40128-3db7-4eac-b324-8c403e5546a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
d00f30ad-28de-4483-9a89-cb8912fec221,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d00f30ad-28de-4483-9a89-cb8912fec221,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d00f30ad-28de-4483-9a89-cb8912fec221,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d00f30ad-28de-4483-9a89-cb8912fec221,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d00f30ad-28de-4483-9a89-cb8912fec221,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d00f30ad-28de-4483-9a89-cb8912fec221,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d00f30ad-28de-4483-9a89-cb8912fec221,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d00f30ad-28de-4483-9a89-cb8912fec221,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d00f30ad-28de-4483-9a89-cb8912fec221,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d00f30ad-28de-4483-9a89-cb8912fec221,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d00f30ad-28de-4483-9a89-cb8912fec221,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d00f30ad-28de-4483-9a89-cb8912fec221,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d00f30ad-28de-4483-9a89-cb8912fec221,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d00f30ad-28de-4483-9a89-cb8912fec221,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d00f30ad-28de-4483-9a89-cb8912fec221,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d00f30ad-28de-4483-9a89-cb8912fec221,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d00f30ad-28de-4483-9a89-cb8912fec221,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
827a2cf5-1b8c-49c5-b82f-c32e1a52f994,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Table 1.17: Hypo- and hyperkalemia summary.,True,Hyper- and Hypokalemia,,,,
ade04dd2-419f-4d36-be9f-14ddae564a8f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"References, resources, and further reading",False,"References, resources, and further reading",,,,
ed9de076-f688-4cd8-a44a-5039bedfba9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,Text,False,Text,,,,
fcf62bf3-be5f-40dd-806c-c7d99829f601,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Burns, Ed, and Robert Buttner. Hypercalcaemia. Lift in the Fast Lane, 2021. https://litfl.com/hypercalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
014e8b4d-75e3-40e4-a899-602a64d5968a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Burns, Ed, and Robert Buttner. Hypocalcaemia. Life in the Fast Lane, 2021. https://litfl.com/hypocalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
9396d0ce-b641-49a1-8331-b97223c1f87d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Buttner, Robert, and Ed Burns. Hyperkalaemia. Life in the Fast Lane. https://litfl.com/hyperkalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
8e416c25-b1b8-4a1b-9f80-99810ecef4c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Buttner, Robert, and Ed Burns. Hypokalaemia. Life in the Fast Lane, 2021. https://litfl.com/hypokalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
128a1f1f-7906-438b-8201-f65035f34d8d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Chhabra, Lovely, Amandeep Goyal, and Michael D. Benham. Wolff Parkinson White Syndrome. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK554437/, CC BY 4.0.",True,Text,,,,
ac383d76-692a-44d2-95dd-af04128f5c7c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Custer, Adam M., Varun S. Yelamanchili, and Sarah L. Lappin. Multifocal Atrial Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459152/, CC BY 4.0.",True,Text,,,,
ad3491ab-28d8-4dc1-9e02-17168671fd4c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Farzam, Khashayar, and John R. Richards. Premature Ventricular Contraction. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532991/, CC BY 4.0.",True,Text,,,,
fdb8d0dd-df25-4e83-a519-d86ba3ed7383,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Foth, Christopher, Manesh Kumar Gangwani, and Heidi Alvey. Ventricular Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532954/, CC BY 4.0.",True,Text,,,,
2c86780a-7773-46a0-b368-66fc5e0bea1e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Hafeez, Yamama, and Shamai A. Grossman. Sinus Bradycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK493201/, CC BY 4.0.",True,Text,,,,
8aa382da-a842-4e03-9f31-bdac9f27cf03,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Harkness, Weston T., and Mary Hicks. Right Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK507872/, CC BY 4.0.",True,Text,,,,
a6612336-0338-4bb6-9dfb-8737ec01d797,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Heaton, Joseph, and Srikanth Yandrapalli. Premature Atrial Contractions. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK559204/, CC BY 4.0.",True,Text,,,,
62b7ec25-d74a-49cf-9562-aabe903c7cb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Kashou, Anthony H., Amandeep Goyal, Tran Nguyen, and Lovely Chhabra. Atrioventricular Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459147/, CC BY 4.0.",True,Text,,,,
5d8a5855-e206-4238-8e81-c703f8e11223,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,“Learn the Heart.” Healio. https://www.healio.com/cardiology/learn-the-heart.,True,Text,,,,
04fae478-acd6-4ce8-a38a-9f0543ee5898,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Ludhwani, Dipesh, Amandeep Goyal, and Mandar Jagtap. Ventricular Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK537120/, CC BY 4.0.",True,Text,,,,
e653cd39-7c55-48de-977f-221af86bd38b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Nesheiwat, Zeid, Amandeep Goyal, and Mandar Jagtap. Atrial Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK526072/, CC BY 4.0.",True,Text,,,,
b8a67f0b-3e2c-4986-a3b7-6ecbf7ba11ef,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Pipilas, Daniel C., Bruce A. Koplan, and Leonard S. Lilly. “The Electrocardiogram.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 4. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
964505d1-d5b8-4ea7-a179-f5e4087933e3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Rodriguez Ziccardi, Mary, Amandeep Goyal, and Christopher V. Maani. Atrial Flutter. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK540985/, CC BY 4.0.",True,Text,,,,
3e2cc667-85e3-4e3a-bf07-5aad74ed3051,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-14,"Scherbak, Dmitriy, and Gregory J. Hicks. Left Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK482167/, CC BY 4.0.",True,Text,,,,
49be0169-c9ff-4937-add9-5e1c23db42e9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,USMLE,False,USMLE,,,,
48911ad7-174c-44f3-b662-5117047e2fb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
48911ad7-174c-44f3-b662-5117047e2fb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
48911ad7-174c-44f3-b662-5117047e2fb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
48911ad7-174c-44f3-b662-5117047e2fb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
48911ad7-174c-44f3-b662-5117047e2fb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
48911ad7-174c-44f3-b662-5117047e2fb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
48911ad7-174c-44f3-b662-5117047e2fb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
48911ad7-174c-44f3-b662-5117047e2fb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
48911ad7-174c-44f3-b662-5117047e2fb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
48911ad7-174c-44f3-b662-5117047e2fb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
48911ad7-174c-44f3-b662-5117047e2fb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
48911ad7-174c-44f3-b662-5117047e2fb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
48911ad7-174c-44f3-b662-5117047e2fb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
48911ad7-174c-44f3-b662-5117047e2fb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
48911ad7-174c-44f3-b662-5117047e2fb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
48911ad7-174c-44f3-b662-5117047e2fb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
48911ad7-174c-44f3-b662-5117047e2fb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
4f1cbc44-7ae0-4ce1-bf06-a4d7f78639dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,10q22,False,10q22,,,,
97afdbd9-15b7-4b4c-9bf4-b75d5ec12b7b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,q24,False,q24,,,,
088a59e4-8128-4d27-9ca0-5fee38c6afec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,fibrillatory,False,fibrillatory,,,,
37e07f46-88b2-4f0e-a040-369730f1dc65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
37e07f46-88b2-4f0e-a040-369730f1dc65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
37e07f46-88b2-4f0e-a040-369730f1dc65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
37e07f46-88b2-4f0e-a040-369730f1dc65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
37e07f46-88b2-4f0e-a040-369730f1dc65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
37e07f46-88b2-4f0e-a040-369730f1dc65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
37e07f46-88b2-4f0e-a040-369730f1dc65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
37e07f46-88b2-4f0e-a040-369730f1dc65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
37e07f46-88b2-4f0e-a040-369730f1dc65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
37e07f46-88b2-4f0e-a040-369730f1dc65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
37e07f46-88b2-4f0e-a040-369730f1dc65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
37e07f46-88b2-4f0e-a040-369730f1dc65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
37e07f46-88b2-4f0e-a040-369730f1dc65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
37e07f46-88b2-4f0e-a040-369730f1dc65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
37e07f46-88b2-4f0e-a040-369730f1dc65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
37e07f46-88b2-4f0e-a040-369730f1dc65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
37e07f46-88b2-4f0e-a040-369730f1dc65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
367938d1-1fe6-404f-8744-c6099a076850,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Table 1.1: Atrial fibrillation summary.,True,fibrillatory,,,,
df99cbfd-8226-4290-977a-3bd00a31598d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Atrial Flutter,False,Atrial Flutter,,,,
25c5bb88-5647-4bc7-a6e9-f04406153700,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
25c5bb88-5647-4bc7-a6e9-f04406153700,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
25c5bb88-5647-4bc7-a6e9-f04406153700,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
25c5bb88-5647-4bc7-a6e9-f04406153700,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
25c5bb88-5647-4bc7-a6e9-f04406153700,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
25c5bb88-5647-4bc7-a6e9-f04406153700,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
25c5bb88-5647-4bc7-a6e9-f04406153700,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
25c5bb88-5647-4bc7-a6e9-f04406153700,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
25c5bb88-5647-4bc7-a6e9-f04406153700,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
25c5bb88-5647-4bc7-a6e9-f04406153700,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
25c5bb88-5647-4bc7-a6e9-f04406153700,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
25c5bb88-5647-4bc7-a6e9-f04406153700,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
25c5bb88-5647-4bc7-a6e9-f04406153700,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
25c5bb88-5647-4bc7-a6e9-f04406153700,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
25c5bb88-5647-4bc7-a6e9-f04406153700,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
25c5bb88-5647-4bc7-a6e9-f04406153700,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
25c5bb88-5647-4bc7-a6e9-f04406153700,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
54ef6047-d4e0-4ac9-a978-42eaa1fa54b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,macroreentrant,False,macroreentrant,,,,
a3ef0666-8a40-4c11-af7b-68acb85e0fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,cavotricuspid,False,cavotricuspid,,,,
c732521a-dc4e-485e-be95-107108ed4186,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"As with atrial fibrillation, the AV node’s refractory period prevents most of the P-waves from progressing to the ventricle, but commonly the AV conduction will be 2-to-1, so with an atrial rate of 300 bpm the ventricular rate will be 150 bpm. Parasympathetic stimulation or changes in AV node refractoriness can modify how many P-waves pass into the ventricle, but the the resultant rhythm is “regularly irregular.” When the heart rate is elevated, then distinguishing flutter from fibrillation becomes challenging and slowing ventricular rate pharmaceutically (adenosine) helps the flutter waves reemerge for a definitive diagnosis to be made.",True,cavotricuspid,,,,
06dd093c-7479-4680-b2d1-736c57917aa8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Table 1.2: Atrial flutter summary.,True,cavotricuspid,,,,
6677f34b-22ba-4672-b057-462310b579f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Multifocal Atrial Tachycardia,False,Multifocal Atrial Tachycardia,,,,
247f1535-4ab6-46ef-97b9-2486598aa924,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
247f1535-4ab6-46ef-97b9-2486598aa924,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
247f1535-4ab6-46ef-97b9-2486598aa924,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
247f1535-4ab6-46ef-97b9-2486598aa924,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
247f1535-4ab6-46ef-97b9-2486598aa924,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
247f1535-4ab6-46ef-97b9-2486598aa924,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
247f1535-4ab6-46ef-97b9-2486598aa924,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
247f1535-4ab6-46ef-97b9-2486598aa924,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
247f1535-4ab6-46ef-97b9-2486598aa924,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
247f1535-4ab6-46ef-97b9-2486598aa924,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
247f1535-4ab6-46ef-97b9-2486598aa924,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
247f1535-4ab6-46ef-97b9-2486598aa924,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
247f1535-4ab6-46ef-97b9-2486598aa924,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
247f1535-4ab6-46ef-97b9-2486598aa924,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
247f1535-4ab6-46ef-97b9-2486598aa924,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
247f1535-4ab6-46ef-97b9-2486598aa924,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
247f1535-4ab6-46ef-97b9-2486598aa924,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
20c69070-1219-4203-b5a9-d48a65bfb755,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"MAT frequently occurs in the setting of severe lung disease and, more specifically, during an exacerbation of lung disease. This rhythm is benign, and once the underlying lung disease is treated, it should resolve.",True,Multifocal Atrial Tachycardia,,,,
543cc4ef-9563-4b8a-bc4e-d7a623e5ca79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Table 1.3: MAT summary.,True,Multifocal Atrial Tachycardia,,,,
1a2145cf-c37f-4538-ab08-e8f0494fa9d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Premature Atrial Contraction,False,Premature Atrial Contraction,,,,
e61a9769-e8e4-4c92-b48e-4b78eda8fa5a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A premature atrial contraction (PAC) is generated by a depolarization instigated outside of the SA node. This produces an extra P-wave, and consequently a shortening from previous P-P intervals is seen. The aberrant P-wave also has a different morphology from a sinus P-wave because of its different anatomical origin.",True,Premature Atrial Contraction,,,,
48dfbb65-b336-42e6-b9b9-1c4bcd50a51b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
48dfbb65-b336-42e6-b9b9-1c4bcd50a51b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
48dfbb65-b336-42e6-b9b9-1c4bcd50a51b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
48dfbb65-b336-42e6-b9b9-1c4bcd50a51b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
48dfbb65-b336-42e6-b9b9-1c4bcd50a51b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
48dfbb65-b336-42e6-b9b9-1c4bcd50a51b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
48dfbb65-b336-42e6-b9b9-1c4bcd50a51b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
48dfbb65-b336-42e6-b9b9-1c4bcd50a51b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
48dfbb65-b336-42e6-b9b9-1c4bcd50a51b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
48dfbb65-b336-42e6-b9b9-1c4bcd50a51b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
48dfbb65-b336-42e6-b9b9-1c4bcd50a51b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
48dfbb65-b336-42e6-b9b9-1c4bcd50a51b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
48dfbb65-b336-42e6-b9b9-1c4bcd50a51b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
48dfbb65-b336-42e6-b9b9-1c4bcd50a51b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
48dfbb65-b336-42e6-b9b9-1c4bcd50a51b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
48dfbb65-b336-42e6-b9b9-1c4bcd50a51b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
48dfbb65-b336-42e6-b9b9-1c4bcd50a51b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
1379e899-87bf-4db1-81ea-4a3132ac78ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"If a PAC occurs when the AV node has not yet recovered from its refractory period, the PAC will fail to conduct to the ventricles; meaning the PAC will not be followed by a QRS complex or the ectopic P-R interval will be prolonged. The ECG will show a premature, ectopic P-wave and then no QRS complex afterward. When this occurs along with bigeminy, the ECG can appear as if there is sinus bradycardia.",True,Premature Atrial Contraction,,,,
4c9348ac-7bce-4f0c-9388-6ece3f2466ed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Table 1.4: PAC summary.,True,Premature Atrial Contraction,,,,
c15d050d-90d7-4c9b-b326-1cfbe9cc9711,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Sinus Bradycardia,False,Sinus Bradycardia,,,,
39b9c56c-53f2-471f-b5b0-de50b8088493,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Sinus bradycardia denotes a sinus rhythm below 60 bpm. Otherwise the ECG waveform is normal on an ECG with an upright P-wave in lead II preceding every QRS complex. There are many intrinsic causes associated with the heart itself, as well as extrinsic causes, some of which are listed table 1.5. Sinus bradycardia is usually asymptomatic as rates of 40–50 bpm can maintain hemodynamic stability. Rates below this can produce symptoms of fatigue, dizziness, and dyspnea on exertion.",True,Sinus Bradycardia,,,,
0c8731fd-4bac-44f8-9759-80756b1643fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Table 1.5: Intrinsic and extrinsic causes associated with the heart.,True,Sinus Bradycardia,,,,
f71ada19-1e35-4cc4-b24b-9bab6f4789bb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Table 1.6: Sinus bradycardia summary.,True,Sinus Bradycardia,,,,
f9b39239-17f2-489f-b390-e8ddac7c157c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Premature Ventricular Contractions,False,Premature Ventricular Contractions,,,,
ed48ec75-f3cf-4d33-bdfc-063787b74f81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
ed48ec75-f3cf-4d33-bdfc-063787b74f81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
ed48ec75-f3cf-4d33-bdfc-063787b74f81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
ed48ec75-f3cf-4d33-bdfc-063787b74f81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
ed48ec75-f3cf-4d33-bdfc-063787b74f81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
ed48ec75-f3cf-4d33-bdfc-063787b74f81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
ed48ec75-f3cf-4d33-bdfc-063787b74f81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
ed48ec75-f3cf-4d33-bdfc-063787b74f81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
ed48ec75-f3cf-4d33-bdfc-063787b74f81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
ed48ec75-f3cf-4d33-bdfc-063787b74f81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
ed48ec75-f3cf-4d33-bdfc-063787b74f81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
ed48ec75-f3cf-4d33-bdfc-063787b74f81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
ed48ec75-f3cf-4d33-bdfc-063787b74f81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
ed48ec75-f3cf-4d33-bdfc-063787b74f81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
ed48ec75-f3cf-4d33-bdfc-063787b74f81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
ed48ec75-f3cf-4d33-bdfc-063787b74f81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
ed48ec75-f3cf-4d33-bdfc-063787b74f81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
dde98ba1-009d-454b-a8c2-e8480114aa62,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Table 1.7: PVC summary.,True,Premature Ventricular Contractions,,,,
94bde2d6-0939-46eb-9b5f-b0576a340222,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Ventricular Tachycardia,False,Ventricular Tachycardia,,,,
a05da61b-7d93-4e87-a54e-abd0241581c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Ventricular tachycardia (VT) is caused by reentry currents being established in the ventricular myocardium or groups of ventricular myocytes that have aberrant electrical behavior. As such, VT is usually caused by underlying cardiac disease.",True,Ventricular Tachycardia,,,,
7605e12e-8b49-4ea1-bf6c-57276c792fb7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Like a PVC, the aberrant depolarizations do not follow the normal conduction pathways so are wide (>120 msecs), but unlike a PVC, VT involves a ventricular rate >100 bpm. With disorganized contractility and reduced filling time, VT can lead to hemodynamic instability and severe hypotension—hence it is life threatening.",True,Ventricular Tachycardia,,,,
1623f8fa-ab90-4988-bd91-34d515b1471a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The QRS morphology in VT is highly variable between patients and depends on where the arrhythmia originates. Consequently there are several ways to classify VT based on duration, symptoms, QRS morphology, rate, and origin.",True,Ventricular Tachycardia,,,,
790787e8-09ac-48e7-b3fa-11cbc2bcb432,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Sustained VT is any VT that lasts for more than 30 seconds or is symptomatic. Nonsustained VT lasts for less than 30 seconds and is asymptomatic.,True,Ventricular Tachycardia,,,,
414f23e6-e14b-4c8d-9b77-6daf7786855e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
414f23e6-e14b-4c8d-9b77-6daf7786855e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
414f23e6-e14b-4c8d-9b77-6daf7786855e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
414f23e6-e14b-4c8d-9b77-6daf7786855e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
414f23e6-e14b-4c8d-9b77-6daf7786855e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
414f23e6-e14b-4c8d-9b77-6daf7786855e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
414f23e6-e14b-4c8d-9b77-6daf7786855e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
414f23e6-e14b-4c8d-9b77-6daf7786855e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
414f23e6-e14b-4c8d-9b77-6daf7786855e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
414f23e6-e14b-4c8d-9b77-6daf7786855e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
414f23e6-e14b-4c8d-9b77-6daf7786855e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
414f23e6-e14b-4c8d-9b77-6daf7786855e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
414f23e6-e14b-4c8d-9b77-6daf7786855e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
414f23e6-e14b-4c8d-9b77-6daf7786855e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
414f23e6-e14b-4c8d-9b77-6daf7786855e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
414f23e6-e14b-4c8d-9b77-6daf7786855e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
414f23e6-e14b-4c8d-9b77-6daf7786855e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
90e4b7c7-8bed-43f4-8f1b-7631202ad32e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
90e4b7c7-8bed-43f4-8f1b-7631202ad32e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
90e4b7c7-8bed-43f4-8f1b-7631202ad32e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
90e4b7c7-8bed-43f4-8f1b-7631202ad32e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
90e4b7c7-8bed-43f4-8f1b-7631202ad32e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
90e4b7c7-8bed-43f4-8f1b-7631202ad32e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
90e4b7c7-8bed-43f4-8f1b-7631202ad32e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
90e4b7c7-8bed-43f4-8f1b-7631202ad32e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
90e4b7c7-8bed-43f4-8f1b-7631202ad32e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
90e4b7c7-8bed-43f4-8f1b-7631202ad32e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
90e4b7c7-8bed-43f4-8f1b-7631202ad32e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
90e4b7c7-8bed-43f4-8f1b-7631202ad32e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
90e4b7c7-8bed-43f4-8f1b-7631202ad32e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
90e4b7c7-8bed-43f4-8f1b-7631202ad32e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
90e4b7c7-8bed-43f4-8f1b-7631202ad32e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
90e4b7c7-8bed-43f4-8f1b-7631202ad32e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
90e4b7c7-8bed-43f4-8f1b-7631202ad32e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
7827fa9a-eeec-41be-aa32-0295681c8709,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Torsades de pointes is associated with a prolonged QT interval (>600 msecs) that helps distinguish it from other forms of polymorphous VT. The longer QT interval can be caused by ionic abnormalities that reduce the repolarizing current of Phase 3 of the cardiac action potential. This makes the myocardium susceptible to early after-depolarizations—the trigger for torsades de pointes. These after-depolarizations do not happen uniformly across the myocardium and are more common in endocardial tissue where the repolarization currents are slower. So torsades de pointes arises from the after-depolarizations causing reentry currents in neighboring tissue.,True,Ventricular Tachycardia,,,,
5da27675-2c9b-42eb-8dbe-efbcc8e82f6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Both common garden variety VTs and torsades de pointes can progress to ventricular fibrillation.,True,Ventricular Tachycardia,,,,
a3ce60f6-c1a9-4de1-a999-00c4c0b2fce3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Table 1.8: VT summary.,True,Ventricular Tachycardia,,,,
24bcfad9-5dc3-45ca-8c93-13b27f1b068a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Ventricular Fibrillation,False,Ventricular Fibrillation,,,,
ba8f4227-b16f-4ebb-b0fa-935ad7952511,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Ventricular fibrillation (VF) occurs when the ventricular rate exceeds 400 bpm. The disorganized and uncoordinated contraction of the myocardium causes cardiac output to fall to catastrophic levels. Rates of survival for out-of-hospital VF are low.,True,Ventricular Fibrillation,,,,
286cb7e2-54fc-4988-a57d-42658d299130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
286cb7e2-54fc-4988-a57d-42658d299130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
286cb7e2-54fc-4988-a57d-42658d299130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
286cb7e2-54fc-4988-a57d-42658d299130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
286cb7e2-54fc-4988-a57d-42658d299130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
286cb7e2-54fc-4988-a57d-42658d299130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
286cb7e2-54fc-4988-a57d-42658d299130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
286cb7e2-54fc-4988-a57d-42658d299130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
286cb7e2-54fc-4988-a57d-42658d299130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
286cb7e2-54fc-4988-a57d-42658d299130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
286cb7e2-54fc-4988-a57d-42658d299130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
286cb7e2-54fc-4988-a57d-42658d299130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
286cb7e2-54fc-4988-a57d-42658d299130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
286cb7e2-54fc-4988-a57d-42658d299130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
286cb7e2-54fc-4988-a57d-42658d299130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
286cb7e2-54fc-4988-a57d-42658d299130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
286cb7e2-54fc-4988-a57d-42658d299130,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
f3397e5d-bd0d-4786-9335-63418df23ece,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Table 1.9: VF summary.,True,Ventricular Fibrillation,,,,
ed2f3df4-f9f8-46c8-85f9-c5d0d6bb4335,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,First-Degree Atrioventricular Block,False,First-Degree Atrioventricular Block,,,,
3b84854b-d132-4cb3-a28b-0cdff085d4cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3b84854b-d132-4cb3-a28b-0cdff085d4cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3b84854b-d132-4cb3-a28b-0cdff085d4cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3b84854b-d132-4cb3-a28b-0cdff085d4cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3b84854b-d132-4cb3-a28b-0cdff085d4cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3b84854b-d132-4cb3-a28b-0cdff085d4cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3b84854b-d132-4cb3-a28b-0cdff085d4cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3b84854b-d132-4cb3-a28b-0cdff085d4cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3b84854b-d132-4cb3-a28b-0cdff085d4cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3b84854b-d132-4cb3-a28b-0cdff085d4cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3b84854b-d132-4cb3-a28b-0cdff085d4cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3b84854b-d132-4cb3-a28b-0cdff085d4cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3b84854b-d132-4cb3-a28b-0cdff085d4cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3b84854b-d132-4cb3-a28b-0cdff085d4cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3b84854b-d132-4cb3-a28b-0cdff085d4cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3b84854b-d132-4cb3-a28b-0cdff085d4cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3b84854b-d132-4cb3-a28b-0cdff085d4cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
cded8b4b-97ca-430e-882e-1647b793e343,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
cded8b4b-97ca-430e-882e-1647b793e343,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
cded8b4b-97ca-430e-882e-1647b793e343,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
cded8b4b-97ca-430e-882e-1647b793e343,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
cded8b4b-97ca-430e-882e-1647b793e343,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
cded8b4b-97ca-430e-882e-1647b793e343,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
cded8b4b-97ca-430e-882e-1647b793e343,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
cded8b4b-97ca-430e-882e-1647b793e343,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
cded8b4b-97ca-430e-882e-1647b793e343,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
cded8b4b-97ca-430e-882e-1647b793e343,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
cded8b4b-97ca-430e-882e-1647b793e343,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
cded8b4b-97ca-430e-882e-1647b793e343,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
cded8b4b-97ca-430e-882e-1647b793e343,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
cded8b4b-97ca-430e-882e-1647b793e343,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
cded8b4b-97ca-430e-882e-1647b793e343,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
cded8b4b-97ca-430e-882e-1647b793e343,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
cded8b4b-97ca-430e-882e-1647b793e343,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ca3a1ff1-1666-4cf6-9b04-c467b7439fb3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Table 1.10: First-degree block summary.,True,First-Degree Atrioventricular Block,,,,
f9eb6373-db42-4465-8c9f-09a3e871f791,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Second-Degree Atrioventricular Block,False,Second-Degree Atrioventricular Block,,,,
ed3113dd-1f15-47c8-8a77-ef48dd8e51d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A second-degree atrioventricular block also has changes in P-R interval, but it starts to show failure of the P-wave to propagate a QRS complex every time (i.e., intermittently the depolarization fails to reach the ventricles). The pattern of missed ventricular depolarizations, or blocked P-waves, is often very regular and described as a ratio of P-waves to QRS complex. The way in which the P-R interval changes in relation to the blocked P-waves produces subclassifications of second-degree blocks, Mobitz I and II.",True,Second-Degree Atrioventricular Block,,,,
7c71977a-8c37-455d-90f9-d95189d3d19c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
7c71977a-8c37-455d-90f9-d95189d3d19c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
7c71977a-8c37-455d-90f9-d95189d3d19c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
7c71977a-8c37-455d-90f9-d95189d3d19c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
7c71977a-8c37-455d-90f9-d95189d3d19c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
7c71977a-8c37-455d-90f9-d95189d3d19c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
7c71977a-8c37-455d-90f9-d95189d3d19c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
7c71977a-8c37-455d-90f9-d95189d3d19c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
7c71977a-8c37-455d-90f9-d95189d3d19c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
7c71977a-8c37-455d-90f9-d95189d3d19c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
7c71977a-8c37-455d-90f9-d95189d3d19c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
7c71977a-8c37-455d-90f9-d95189d3d19c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
7c71977a-8c37-455d-90f9-d95189d3d19c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
7c71977a-8c37-455d-90f9-d95189d3d19c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
7c71977a-8c37-455d-90f9-d95189d3d19c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
7c71977a-8c37-455d-90f9-d95189d3d19c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
7c71977a-8c37-455d-90f9-d95189d3d19c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
ec5c9ac5-1765-40a9-9315-187d4bee65fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
ec5c9ac5-1765-40a9-9315-187d4bee65fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
ec5c9ac5-1765-40a9-9315-187d4bee65fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
ec5c9ac5-1765-40a9-9315-187d4bee65fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
ec5c9ac5-1765-40a9-9315-187d4bee65fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
ec5c9ac5-1765-40a9-9315-187d4bee65fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
ec5c9ac5-1765-40a9-9315-187d4bee65fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
ec5c9ac5-1765-40a9-9315-187d4bee65fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
ec5c9ac5-1765-40a9-9315-187d4bee65fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
ec5c9ac5-1765-40a9-9315-187d4bee65fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
ec5c9ac5-1765-40a9-9315-187d4bee65fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
ec5c9ac5-1765-40a9-9315-187d4bee65fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
ec5c9ac5-1765-40a9-9315-187d4bee65fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
ec5c9ac5-1765-40a9-9315-187d4bee65fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
ec5c9ac5-1765-40a9-9315-187d4bee65fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
ec5c9ac5-1765-40a9-9315-187d4bee65fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
ec5c9ac5-1765-40a9-9315-187d4bee65fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
e4a1feb9-96dc-4fa2-948d-e713def0af43,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Table 1.11: Second-degree block summary.,True,Second-Degree Atrioventricular Block,,,,
ba3a9bf5-df9e-4382-b5e7-000cc02629c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Third-Degree Atrioventricular Block,False,Third-Degree Atrioventricular Block,,,,
de60eb5d-a7b9-46b8-ae20-967df22c42e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
de60eb5d-a7b9-46b8-ae20-967df22c42e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
de60eb5d-a7b9-46b8-ae20-967df22c42e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
de60eb5d-a7b9-46b8-ae20-967df22c42e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
de60eb5d-a7b9-46b8-ae20-967df22c42e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
de60eb5d-a7b9-46b8-ae20-967df22c42e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
de60eb5d-a7b9-46b8-ae20-967df22c42e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
de60eb5d-a7b9-46b8-ae20-967df22c42e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
de60eb5d-a7b9-46b8-ae20-967df22c42e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
de60eb5d-a7b9-46b8-ae20-967df22c42e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
de60eb5d-a7b9-46b8-ae20-967df22c42e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
de60eb5d-a7b9-46b8-ae20-967df22c42e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
de60eb5d-a7b9-46b8-ae20-967df22c42e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
de60eb5d-a7b9-46b8-ae20-967df22c42e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
de60eb5d-a7b9-46b8-ae20-967df22c42e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
de60eb5d-a7b9-46b8-ae20-967df22c42e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
de60eb5d-a7b9-46b8-ae20-967df22c42e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
838b80f0-ddbf-4cd2-a2d3-d3e13b8f0848,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Table 1.12: Third-degree block summary.,True,Third-Degree Atrioventricular Block,,,,
18893616-9361-4caf-953d-fba530463262,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Left Bundle Branch Block,False,Left Bundle Branch Block,,,,
f43ac8a1-74ac-4fc6-90aa-fe8343381918,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"A left bundle branch block (LBBB) is generated when the conductivity of the His-Purkinje system in the left ventricle is compromised, either through damage or disease. The ECG changes, and criteria for LBBB relate to these changes in conductivity and the left-side location.",True,Left Bundle Branch Block,,,,
5bc2af0a-e7aa-4353-ab32-73878a9a701b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5bc2af0a-e7aa-4353-ab32-73878a9a701b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5bc2af0a-e7aa-4353-ab32-73878a9a701b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5bc2af0a-e7aa-4353-ab32-73878a9a701b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5bc2af0a-e7aa-4353-ab32-73878a9a701b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5bc2af0a-e7aa-4353-ab32-73878a9a701b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5bc2af0a-e7aa-4353-ab32-73878a9a701b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5bc2af0a-e7aa-4353-ab32-73878a9a701b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5bc2af0a-e7aa-4353-ab32-73878a9a701b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5bc2af0a-e7aa-4353-ab32-73878a9a701b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5bc2af0a-e7aa-4353-ab32-73878a9a701b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5bc2af0a-e7aa-4353-ab32-73878a9a701b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5bc2af0a-e7aa-4353-ab32-73878a9a701b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5bc2af0a-e7aa-4353-ab32-73878a9a701b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5bc2af0a-e7aa-4353-ab32-73878a9a701b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5bc2af0a-e7aa-4353-ab32-73878a9a701b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5bc2af0a-e7aa-4353-ab32-73878a9a701b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
2c14270d-474c-4f56-814b-857536e58283,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The lateral leads (I, V5, and V6) normally show a downward deflecting Q-wave as normal septal deflection initially occurs left-to-right (i.e., away from the lateral leads). In LBBB the change in direction to right-to-left, plus the longer duration, eliminates the Q-wave from the lateral leads, and Q-waves will be small in aVL.",True,Left Bundle Branch Block,,,,
4a680892-24c2-4faa-95d1-b84cd112703c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4a680892-24c2-4faa-95d1-b84cd112703c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4a680892-24c2-4faa-95d1-b84cd112703c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4a680892-24c2-4faa-95d1-b84cd112703c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4a680892-24c2-4faa-95d1-b84cd112703c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4a680892-24c2-4faa-95d1-b84cd112703c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4a680892-24c2-4faa-95d1-b84cd112703c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4a680892-24c2-4faa-95d1-b84cd112703c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4a680892-24c2-4faa-95d1-b84cd112703c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4a680892-24c2-4faa-95d1-b84cd112703c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4a680892-24c2-4faa-95d1-b84cd112703c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4a680892-24c2-4faa-95d1-b84cd112703c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4a680892-24c2-4faa-95d1-b84cd112703c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4a680892-24c2-4faa-95d1-b84cd112703c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4a680892-24c2-4faa-95d1-b84cd112703c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4a680892-24c2-4faa-95d1-b84cd112703c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4a680892-24c2-4faa-95d1-b84cd112703c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
6cca5645-bdfe-47d4-be9e-09ed4868255a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
6cca5645-bdfe-47d4-be9e-09ed4868255a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
6cca5645-bdfe-47d4-be9e-09ed4868255a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
6cca5645-bdfe-47d4-be9e-09ed4868255a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
6cca5645-bdfe-47d4-be9e-09ed4868255a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
6cca5645-bdfe-47d4-be9e-09ed4868255a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
6cca5645-bdfe-47d4-be9e-09ed4868255a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
6cca5645-bdfe-47d4-be9e-09ed4868255a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
6cca5645-bdfe-47d4-be9e-09ed4868255a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
6cca5645-bdfe-47d4-be9e-09ed4868255a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
6cca5645-bdfe-47d4-be9e-09ed4868255a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
6cca5645-bdfe-47d4-be9e-09ed4868255a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
6cca5645-bdfe-47d4-be9e-09ed4868255a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
6cca5645-bdfe-47d4-be9e-09ed4868255a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
6cca5645-bdfe-47d4-be9e-09ed4868255a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
6cca5645-bdfe-47d4-be9e-09ed4868255a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
6cca5645-bdfe-47d4-be9e-09ed4868255a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c211bc29-e570-4af9-a617-83fd14e340f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Table 1.13: LBBB summary.,True,Left Bundle Branch Block,,,,
27fed7ba-2f56-4d45-8d8d-7a59d471ee98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Right Bundle Branch Block,False,Right Bundle Branch Block,,,,
e0a1b5c1-a112-4aab-a9b8-f413fe00cb55,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The causes and manifestations of a right bundle branch block (RBBB) bear some similarities to those described for LBBB, but of course this time its depolarization of the right ventricle is delayed. Causes of RBBB include ischemic heart disease again as well as other myocardial diseases, but pulmonary issues such as pulmonary embolism and cor pulmonale can be added to the list.",True,Right Bundle Branch Block,,,,
6d9b87a9-ca0a-4185-ae00-d431d39f48d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
6d9b87a9-ca0a-4185-ae00-d431d39f48d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
6d9b87a9-ca0a-4185-ae00-d431d39f48d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
6d9b87a9-ca0a-4185-ae00-d431d39f48d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
6d9b87a9-ca0a-4185-ae00-d431d39f48d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
6d9b87a9-ca0a-4185-ae00-d431d39f48d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
6d9b87a9-ca0a-4185-ae00-d431d39f48d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
6d9b87a9-ca0a-4185-ae00-d431d39f48d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
6d9b87a9-ca0a-4185-ae00-d431d39f48d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
6d9b87a9-ca0a-4185-ae00-d431d39f48d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
6d9b87a9-ca0a-4185-ae00-d431d39f48d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
6d9b87a9-ca0a-4185-ae00-d431d39f48d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
6d9b87a9-ca0a-4185-ae00-d431d39f48d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
6d9b87a9-ca0a-4185-ae00-d431d39f48d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
6d9b87a9-ca0a-4185-ae00-d431d39f48d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
6d9b87a9-ca0a-4185-ae00-d431d39f48d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
6d9b87a9-ca0a-4185-ae00-d431d39f48d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
a53232fa-6491-4856-8da4-802146a1241f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Table 1.14: RBBB summary.,True,Right Bundle Branch Block,,,,
c1d05aa1-f6b4-4225-a899-c890676596e5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Wolff-Parkinson-White Syndrome,False,Wolff-Parkinson-White Syndrome,,,,
aff46e7b-1eca-4923-b6a8-2227bb17f2a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Normally the only electrical connection between the atria and the ventricles is the AV node. Otherwise the fibrous skeleton of the heart electrically insulates the atria from the ventricles. In Wolff-Parkinson-White (WPW) syndrome, that insulation is incomplete, and an “accessory pathway” connects the electrical system of the atria directly to the ventricles. If you think of the AV node as a bridge over the fibrous wall with regulated access, the accessory pathway is like a pathological tunnel under it with no regulation.",True,Wolff-Parkinson-White Syndrome,,,,
41e05ed5-aa83-4094-a46e-9e907d56002f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41e05ed5-aa83-4094-a46e-9e907d56002f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41e05ed5-aa83-4094-a46e-9e907d56002f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41e05ed5-aa83-4094-a46e-9e907d56002f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41e05ed5-aa83-4094-a46e-9e907d56002f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41e05ed5-aa83-4094-a46e-9e907d56002f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41e05ed5-aa83-4094-a46e-9e907d56002f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41e05ed5-aa83-4094-a46e-9e907d56002f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41e05ed5-aa83-4094-a46e-9e907d56002f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41e05ed5-aa83-4094-a46e-9e907d56002f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41e05ed5-aa83-4094-a46e-9e907d56002f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41e05ed5-aa83-4094-a46e-9e907d56002f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41e05ed5-aa83-4094-a46e-9e907d56002f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41e05ed5-aa83-4094-a46e-9e907d56002f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41e05ed5-aa83-4094-a46e-9e907d56002f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41e05ed5-aa83-4094-a46e-9e907d56002f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41e05ed5-aa83-4094-a46e-9e907d56002f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
39a6e384-2b3d-423b-8a4c-68633551a844,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"WPW syndrome is often asymptomatic, and patients do not require immediate treatment. However, if atrial fibrillation occurs in a WPW patient, the accessory pathway can allow the atrial fibrillation waves through to the ventricle (with no AV nodal refractory period to prevent them). Consequently a high ventricular rate is seen, and the risk of ventricular fibrillation being established means immediate clinical attention is required.",True,Wolff-Parkinson-White Syndrome,,,,
b2d84d94-d248-4843-b9fc-b2f65d8d4983,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Hyper- and Hypocalcemia,False,Hyper- and Hypocalcemia,,,,
c22f4e3e-e0aa-4860-8c8a-7cdd16d8634a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
c22f4e3e-e0aa-4860-8c8a-7cdd16d8634a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
c22f4e3e-e0aa-4860-8c8a-7cdd16d8634a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
c22f4e3e-e0aa-4860-8c8a-7cdd16d8634a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
c22f4e3e-e0aa-4860-8c8a-7cdd16d8634a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
c22f4e3e-e0aa-4860-8c8a-7cdd16d8634a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
c22f4e3e-e0aa-4860-8c8a-7cdd16d8634a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
c22f4e3e-e0aa-4860-8c8a-7cdd16d8634a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
c22f4e3e-e0aa-4860-8c8a-7cdd16d8634a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
c22f4e3e-e0aa-4860-8c8a-7cdd16d8634a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
c22f4e3e-e0aa-4860-8c8a-7cdd16d8634a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
c22f4e3e-e0aa-4860-8c8a-7cdd16d8634a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
c22f4e3e-e0aa-4860-8c8a-7cdd16d8634a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
c22f4e3e-e0aa-4860-8c8a-7cdd16d8634a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
c22f4e3e-e0aa-4860-8c8a-7cdd16d8634a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
c22f4e3e-e0aa-4860-8c8a-7cdd16d8634a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
c22f4e3e-e0aa-4860-8c8a-7cdd16d8634a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
fa28957f-62d4-4f99-a287-647c9438a6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
fa28957f-62d4-4f99-a287-647c9438a6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
fa28957f-62d4-4f99-a287-647c9438a6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
fa28957f-62d4-4f99-a287-647c9438a6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
fa28957f-62d4-4f99-a287-647c9438a6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
fa28957f-62d4-4f99-a287-647c9438a6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
fa28957f-62d4-4f99-a287-647c9438a6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
fa28957f-62d4-4f99-a287-647c9438a6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
fa28957f-62d4-4f99-a287-647c9438a6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
fa28957f-62d4-4f99-a287-647c9438a6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
fa28957f-62d4-4f99-a287-647c9438a6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
fa28957f-62d4-4f99-a287-647c9438a6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
fa28957f-62d4-4f99-a287-647c9438a6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
fa28957f-62d4-4f99-a287-647c9438a6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
fa28957f-62d4-4f99-a287-647c9438a6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
fa28957f-62d4-4f99-a287-647c9438a6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
fa28957f-62d4-4f99-a287-647c9438a6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
a84ed926-555e-4bb8-9973-b0cf32b150c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Table 1.16: Hyper- and hypocalcemia summary.,True,Hyper- and Hypocalcemia,,,,
d7acdd15-4578-4143-8c66-eae0d2141574,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Hyper- and Hypokalemia,False,Hyper- and Hypokalemia,,,,
f7a962f3-9cff-47fe-8a2d-016e1c216b90,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"The pathophysiology is not as simple as changes in extracellular K+ changing the electrochemical gradient for K+. Because of potassium’s role in maintaining the resting membrane potential, shifts in extracellular potassium can also influence the activity of Na+ and Ca++ channels.",True,Hyper- and Hypokalemia,,,,
b2442d5a-54ee-4bf0-85cf-fa7c08652c06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
b2442d5a-54ee-4bf0-85cf-fa7c08652c06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
b2442d5a-54ee-4bf0-85cf-fa7c08652c06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
b2442d5a-54ee-4bf0-85cf-fa7c08652c06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
b2442d5a-54ee-4bf0-85cf-fa7c08652c06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
b2442d5a-54ee-4bf0-85cf-fa7c08652c06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
b2442d5a-54ee-4bf0-85cf-fa7c08652c06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
b2442d5a-54ee-4bf0-85cf-fa7c08652c06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
b2442d5a-54ee-4bf0-85cf-fa7c08652c06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
b2442d5a-54ee-4bf0-85cf-fa7c08652c06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
b2442d5a-54ee-4bf0-85cf-fa7c08652c06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
b2442d5a-54ee-4bf0-85cf-fa7c08652c06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
b2442d5a-54ee-4bf0-85cf-fa7c08652c06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
b2442d5a-54ee-4bf0-85cf-fa7c08652c06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
b2442d5a-54ee-4bf0-85cf-fa7c08652c06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
b2442d5a-54ee-4bf0-85cf-fa7c08652c06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
b2442d5a-54ee-4bf0-85cf-fa7c08652c06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
a6055f08-ab3d-4aa6-9ae7-a7fc6aedffc9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"As hypokalemia also inhibits Na+-K+ ATPase, Na+ accumulates inside the cell. This in turn leads to an accumulation of Ca++ because of a subsequent failure of the Na+-Ca++ exchanger. Extended presence of these two positive ions inside the myocyte prolongs the action potential and may manifest as an increased width and amplitude of the P-wave.",True,Hyper- and Hypokalemia,,,,
9930dd9d-a863-406a-90af-38f465f474fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"As hypokalemia worsens, the problems with K+ conductance and repolarization increase, and the myocardium becomes susceptible to early after-depolarization (EAD) arrhythmias.",True,Hyper- and Hypokalemia,,,,
c394eafa-010b-442e-aa97-a1e8ea9b375c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
c394eafa-010b-442e-aa97-a1e8ea9b375c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
c394eafa-010b-442e-aa97-a1e8ea9b375c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
c394eafa-010b-442e-aa97-a1e8ea9b375c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
c394eafa-010b-442e-aa97-a1e8ea9b375c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
c394eafa-010b-442e-aa97-a1e8ea9b375c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
c394eafa-010b-442e-aa97-a1e8ea9b375c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
c394eafa-010b-442e-aa97-a1e8ea9b375c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
c394eafa-010b-442e-aa97-a1e8ea9b375c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
c394eafa-010b-442e-aa97-a1e8ea9b375c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
c394eafa-010b-442e-aa97-a1e8ea9b375c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
c394eafa-010b-442e-aa97-a1e8ea9b375c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
c394eafa-010b-442e-aa97-a1e8ea9b375c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
c394eafa-010b-442e-aa97-a1e8ea9b375c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
c394eafa-010b-442e-aa97-a1e8ea9b375c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
c394eafa-010b-442e-aa97-a1e8ea9b375c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
c394eafa-010b-442e-aa97-a1e8ea9b375c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
84b8f852-c241-43e7-a431-ab0a2541622f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
84b8f852-c241-43e7-a431-ab0a2541622f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
84b8f852-c241-43e7-a431-ab0a2541622f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
84b8f852-c241-43e7-a431-ab0a2541622f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
84b8f852-c241-43e7-a431-ab0a2541622f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
84b8f852-c241-43e7-a431-ab0a2541622f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
84b8f852-c241-43e7-a431-ab0a2541622f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
84b8f852-c241-43e7-a431-ab0a2541622f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
84b8f852-c241-43e7-a431-ab0a2541622f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
84b8f852-c241-43e7-a431-ab0a2541622f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
84b8f852-c241-43e7-a431-ab0a2541622f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
84b8f852-c241-43e7-a431-ab0a2541622f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
84b8f852-c241-43e7-a431-ab0a2541622f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
84b8f852-c241-43e7-a431-ab0a2541622f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
84b8f852-c241-43e7-a431-ab0a2541622f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
84b8f852-c241-43e7-a431-ab0a2541622f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
84b8f852-c241-43e7-a431-ab0a2541622f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
80870824-943a-414d-a909-5c3ffd2f4f2e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
80870824-943a-414d-a909-5c3ffd2f4f2e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
80870824-943a-414d-a909-5c3ffd2f4f2e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
80870824-943a-414d-a909-5c3ffd2f4f2e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
80870824-943a-414d-a909-5c3ffd2f4f2e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
80870824-943a-414d-a909-5c3ffd2f4f2e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
80870824-943a-414d-a909-5c3ffd2f4f2e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
80870824-943a-414d-a909-5c3ffd2f4f2e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
80870824-943a-414d-a909-5c3ffd2f4f2e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
80870824-943a-414d-a909-5c3ffd2f4f2e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
80870824-943a-414d-a909-5c3ffd2f4f2e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
80870824-943a-414d-a909-5c3ffd2f4f2e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
80870824-943a-414d-a909-5c3ffd2f4f2e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
80870824-943a-414d-a909-5c3ffd2f4f2e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
80870824-943a-414d-a909-5c3ffd2f4f2e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
80870824-943a-414d-a909-5c3ffd2f4f2e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
80870824-943a-414d-a909-5c3ffd2f4f2e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
97431e78-d5d9-4522-81b2-9ba50b656008,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97431e78-d5d9-4522-81b2-9ba50b656008,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97431e78-d5d9-4522-81b2-9ba50b656008,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97431e78-d5d9-4522-81b2-9ba50b656008,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97431e78-d5d9-4522-81b2-9ba50b656008,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97431e78-d5d9-4522-81b2-9ba50b656008,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97431e78-d5d9-4522-81b2-9ba50b656008,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97431e78-d5d9-4522-81b2-9ba50b656008,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97431e78-d5d9-4522-81b2-9ba50b656008,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97431e78-d5d9-4522-81b2-9ba50b656008,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97431e78-d5d9-4522-81b2-9ba50b656008,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97431e78-d5d9-4522-81b2-9ba50b656008,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97431e78-d5d9-4522-81b2-9ba50b656008,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97431e78-d5d9-4522-81b2-9ba50b656008,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97431e78-d5d9-4522-81b2-9ba50b656008,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97431e78-d5d9-4522-81b2-9ba50b656008,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
97431e78-d5d9-4522-81b2-9ba50b656008,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
0ee5affd-7287-4ee3-9fec-b5bd1c8a5eb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Table 1.17: Hypo- and hyperkalemia summary.,True,Hyper- and Hypokalemia,,,,
293f0364-e697-42af-9f3c-402c1cb2be25,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"References, resources, and further reading",False,"References, resources, and further reading",,,,
325c58f2-59dc-42bc-9c56-675d5a9caa26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,Text,False,Text,,,,
030b58ad-1766-4324-a6f2-875a0d75ff91,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Burns, Ed, and Robert Buttner. Hypercalcaemia. Lift in the Fast Lane, 2021. https://litfl.com/hypercalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
9dfd0bb6-051e-4ff9-a745-6d8e57a5dd23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Burns, Ed, and Robert Buttner. Hypocalcaemia. Life in the Fast Lane, 2021. https://litfl.com/hypocalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
99828e22-7983-4409-b67f-b3373b69b823,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Buttner, Robert, and Ed Burns. Hyperkalaemia. Life in the Fast Lane. https://litfl.com/hyperkalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
0beb63f1-05ff-488b-90d1-3febebc994be,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Buttner, Robert, and Ed Burns. Hypokalaemia. Life in the Fast Lane, 2021. https://litfl.com/hypokalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
f682832e-b3af-4cd3-9069-53d790f10ef3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Chhabra, Lovely, Amandeep Goyal, and Michael D. Benham. Wolff Parkinson White Syndrome. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK554437/, CC BY 4.0.",True,Text,,,,
2308f03b-4d0e-4179-aac9-6ebb18054849,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Custer, Adam M., Varun S. Yelamanchili, and Sarah L. Lappin. Multifocal Atrial Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459152/, CC BY 4.0.",True,Text,,,,
bfd52e86-5261-4ded-b5b6-03cb13ed2766,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Farzam, Khashayar, and John R. Richards. Premature Ventricular Contraction. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532991/, CC BY 4.0.",True,Text,,,,
e842c3f6-58a3-4515-9545-7f96c9337c1c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Foth, Christopher, Manesh Kumar Gangwani, and Heidi Alvey. Ventricular Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532954/, CC BY 4.0.",True,Text,,,,
cec30542-2ff9-4a55-a154-d33efa0438a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Hafeez, Yamama, and Shamai A. Grossman. Sinus Bradycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK493201/, CC BY 4.0.",True,Text,,,,
8cce9c76-1212-414b-94de-b6de532876c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Harkness, Weston T., and Mary Hicks. Right Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK507872/, CC BY 4.0.",True,Text,,,,
0562116f-d2ca-4a26-bde8-ac904810f55b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Heaton, Joseph, and Srikanth Yandrapalli. Premature Atrial Contractions. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK559204/, CC BY 4.0.",True,Text,,,,
48e598ee-17dd-4f28-86b6-d3bc44f1f583,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Kashou, Anthony H., Amandeep Goyal, Tran Nguyen, and Lovely Chhabra. Atrioventricular Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459147/, CC BY 4.0.",True,Text,,,,
2d0d889e-8bcb-490f-877e-c44f9f404306,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,“Learn the Heart.” Healio. https://www.healio.com/cardiology/learn-the-heart.,True,Text,,,,
722f428c-59e4-441a-a9a2-6ba9f6335ad4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Ludhwani, Dipesh, Amandeep Goyal, and Mandar Jagtap. Ventricular Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK537120/, CC BY 4.0.",True,Text,,,,
d2c2a4c0-15a8-4c60-9868-7ad7ba899e6b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Nesheiwat, Zeid, Amandeep Goyal, and Mandar Jagtap. Atrial Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK526072/, CC BY 4.0.",True,Text,,,,
89877e3a-3cc8-41de-abf3-2d25fae837a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Pipilas, Daniel C., Bruce A. Koplan, and Leonard S. Lilly. “The Electrocardiogram.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 4. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
ed090831-b5ee-4c19-81f5-4ad75b574ed0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Rodriguez Ziccardi, Mary, Amandeep Goyal, and Christopher V. Maani. Atrial Flutter. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK540985/, CC BY 4.0.",True,Text,,,,
1412ccac-4483-4ac0-851e-a4a63d5ef98c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-13,"Scherbak, Dmitriy, and Gregory J. Hicks. Left Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK482167/, CC BY 4.0.",True,Text,,,,
f80267b0-a24f-48df-a4c7-bd747afd31c9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,USMLE,False,USMLE,,,,
5a294efe-cd68-4088-9436-382432fab764,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5a294efe-cd68-4088-9436-382432fab764,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5a294efe-cd68-4088-9436-382432fab764,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5a294efe-cd68-4088-9436-382432fab764,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5a294efe-cd68-4088-9436-382432fab764,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5a294efe-cd68-4088-9436-382432fab764,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5a294efe-cd68-4088-9436-382432fab764,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5a294efe-cd68-4088-9436-382432fab764,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5a294efe-cd68-4088-9436-382432fab764,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5a294efe-cd68-4088-9436-382432fab764,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5a294efe-cd68-4088-9436-382432fab764,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5a294efe-cd68-4088-9436-382432fab764,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5a294efe-cd68-4088-9436-382432fab764,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5a294efe-cd68-4088-9436-382432fab764,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5a294efe-cd68-4088-9436-382432fab764,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5a294efe-cd68-4088-9436-382432fab764,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5a294efe-cd68-4088-9436-382432fab764,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
800f5d7a-21f8-499e-8a56-42a806c1e1bf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,10q22,False,10q22,,,,
5e7e4460-43ab-438c-a96f-f6d0a3c388c1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,q24,False,q24,,,,
fa39f188-2844-4a7b-848d-e86bee01f1be,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,fibrillatory,False,fibrillatory,,,,
e66bb29d-037c-4965-af7c-e298228798d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
e66bb29d-037c-4965-af7c-e298228798d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
e66bb29d-037c-4965-af7c-e298228798d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
e66bb29d-037c-4965-af7c-e298228798d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
e66bb29d-037c-4965-af7c-e298228798d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
e66bb29d-037c-4965-af7c-e298228798d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
e66bb29d-037c-4965-af7c-e298228798d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
e66bb29d-037c-4965-af7c-e298228798d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
e66bb29d-037c-4965-af7c-e298228798d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
e66bb29d-037c-4965-af7c-e298228798d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
e66bb29d-037c-4965-af7c-e298228798d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
e66bb29d-037c-4965-af7c-e298228798d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
e66bb29d-037c-4965-af7c-e298228798d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
e66bb29d-037c-4965-af7c-e298228798d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
e66bb29d-037c-4965-af7c-e298228798d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
e66bb29d-037c-4965-af7c-e298228798d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
e66bb29d-037c-4965-af7c-e298228798d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
545d2f99-5e76-4290-8193-e48a29c46d53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Table 1.1: Atrial fibrillation summary.,True,fibrillatory,,,,
b768e064-d15a-469d-a4da-309d2f3ab7d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Atrial Flutter,False,Atrial Flutter,,,,
107b0a01-509b-42d8-ab61-275452f0b94e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
107b0a01-509b-42d8-ab61-275452f0b94e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
107b0a01-509b-42d8-ab61-275452f0b94e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
107b0a01-509b-42d8-ab61-275452f0b94e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
107b0a01-509b-42d8-ab61-275452f0b94e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
107b0a01-509b-42d8-ab61-275452f0b94e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
107b0a01-509b-42d8-ab61-275452f0b94e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
107b0a01-509b-42d8-ab61-275452f0b94e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
107b0a01-509b-42d8-ab61-275452f0b94e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
107b0a01-509b-42d8-ab61-275452f0b94e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
107b0a01-509b-42d8-ab61-275452f0b94e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
107b0a01-509b-42d8-ab61-275452f0b94e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
107b0a01-509b-42d8-ab61-275452f0b94e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
107b0a01-509b-42d8-ab61-275452f0b94e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
107b0a01-509b-42d8-ab61-275452f0b94e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
107b0a01-509b-42d8-ab61-275452f0b94e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
107b0a01-509b-42d8-ab61-275452f0b94e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
e8a54dce-74a9-44ad-8647-c9c0ab47f1ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,macroreentrant,False,macroreentrant,,,,
3e60a963-b4c0-4baf-99a6-925e48e1b35b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,cavotricuspid,False,cavotricuspid,,,,
5283c9d6-962d-4e03-b2a0-85cf1b8355cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"As with atrial fibrillation, the AV node’s refractory period prevents most of the P-waves from progressing to the ventricle, but commonly the AV conduction will be 2-to-1, so with an atrial rate of 300 bpm the ventricular rate will be 150 bpm. Parasympathetic stimulation or changes in AV node refractoriness can modify how many P-waves pass into the ventricle, but the the resultant rhythm is “regularly irregular.” When the heart rate is elevated, then distinguishing flutter from fibrillation becomes challenging and slowing ventricular rate pharmaceutically (adenosine) helps the flutter waves reemerge for a definitive diagnosis to be made.",True,cavotricuspid,,,,
b41162b3-6b90-41f7-b82e-ae411906416f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Table 1.2: Atrial flutter summary.,True,cavotricuspid,,,,
37dd7041-33bf-4d6f-b708-99d238eb7ef8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Multifocal Atrial Tachycardia,False,Multifocal Atrial Tachycardia,,,,
428d4778-9383-48f1-981e-e396e98b23db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
428d4778-9383-48f1-981e-e396e98b23db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
428d4778-9383-48f1-981e-e396e98b23db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
428d4778-9383-48f1-981e-e396e98b23db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
428d4778-9383-48f1-981e-e396e98b23db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
428d4778-9383-48f1-981e-e396e98b23db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
428d4778-9383-48f1-981e-e396e98b23db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
428d4778-9383-48f1-981e-e396e98b23db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
428d4778-9383-48f1-981e-e396e98b23db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
428d4778-9383-48f1-981e-e396e98b23db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
428d4778-9383-48f1-981e-e396e98b23db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
428d4778-9383-48f1-981e-e396e98b23db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
428d4778-9383-48f1-981e-e396e98b23db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
428d4778-9383-48f1-981e-e396e98b23db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
428d4778-9383-48f1-981e-e396e98b23db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
428d4778-9383-48f1-981e-e396e98b23db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
428d4778-9383-48f1-981e-e396e98b23db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
d9ae0b1e-7355-4545-bf7f-d518b2efd2f3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"MAT frequently occurs in the setting of severe lung disease and, more specifically, during an exacerbation of lung disease. This rhythm is benign, and once the underlying lung disease is treated, it should resolve.",True,Multifocal Atrial Tachycardia,,,,
ab5904dc-8d94-4cad-a8e6-4fe6f3bcf608,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Table 1.3: MAT summary.,True,Multifocal Atrial Tachycardia,,,,
f1ba75c5-4e74-4851-bc50-13e31349a90f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Premature Atrial Contraction,False,Premature Atrial Contraction,,,,
1d3af0c7-fb8c-43a9-a8bf-f465be59add3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A premature atrial contraction (PAC) is generated by a depolarization instigated outside of the SA node. This produces an extra P-wave, and consequently a shortening from previous P-P intervals is seen. The aberrant P-wave also has a different morphology from a sinus P-wave because of its different anatomical origin.",True,Premature Atrial Contraction,,,,
4d969610-7c7a-47b7-b85a-3ceafdb834da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
4d969610-7c7a-47b7-b85a-3ceafdb834da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
4d969610-7c7a-47b7-b85a-3ceafdb834da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
4d969610-7c7a-47b7-b85a-3ceafdb834da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
4d969610-7c7a-47b7-b85a-3ceafdb834da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
4d969610-7c7a-47b7-b85a-3ceafdb834da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
4d969610-7c7a-47b7-b85a-3ceafdb834da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
4d969610-7c7a-47b7-b85a-3ceafdb834da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
4d969610-7c7a-47b7-b85a-3ceafdb834da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
4d969610-7c7a-47b7-b85a-3ceafdb834da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
4d969610-7c7a-47b7-b85a-3ceafdb834da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
4d969610-7c7a-47b7-b85a-3ceafdb834da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
4d969610-7c7a-47b7-b85a-3ceafdb834da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
4d969610-7c7a-47b7-b85a-3ceafdb834da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
4d969610-7c7a-47b7-b85a-3ceafdb834da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
4d969610-7c7a-47b7-b85a-3ceafdb834da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
4d969610-7c7a-47b7-b85a-3ceafdb834da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
ad468119-2821-4106-8659-adbb5e4e2a06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"If a PAC occurs when the AV node has not yet recovered from its refractory period, the PAC will fail to conduct to the ventricles; meaning the PAC will not be followed by a QRS complex or the ectopic P-R interval will be prolonged. The ECG will show a premature, ectopic P-wave and then no QRS complex afterward. When this occurs along with bigeminy, the ECG can appear as if there is sinus bradycardia.",True,Premature Atrial Contraction,,,,
4b4bd12b-c4c1-40e4-80d5-c00a5661d9b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Table 1.4: PAC summary.,True,Premature Atrial Contraction,,,,
2c385f5e-15bd-44fd-980f-f9a8260d4108,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Sinus Bradycardia,False,Sinus Bradycardia,,,,
a5d6c8ab-34ba-4578-b140-c45ed655602a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Sinus bradycardia denotes a sinus rhythm below 60 bpm. Otherwise the ECG waveform is normal on an ECG with an upright P-wave in lead II preceding every QRS complex. There are many intrinsic causes associated with the heart itself, as well as extrinsic causes, some of which are listed table 1.5. Sinus bradycardia is usually asymptomatic as rates of 40–50 bpm can maintain hemodynamic stability. Rates below this can produce symptoms of fatigue, dizziness, and dyspnea on exertion.",True,Sinus Bradycardia,,,,
68e1ad5c-f07d-4998-a2f2-d5118c4d6af0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Table 1.5: Intrinsic and extrinsic causes associated with the heart.,True,Sinus Bradycardia,,,,
42a8b954-9552-475a-a2b6-848fb23b4f33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Table 1.6: Sinus bradycardia summary.,True,Sinus Bradycardia,,,,
5c7d35f1-d19f-4d93-b14f-472c066a583d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Premature Ventricular Contractions,False,Premature Ventricular Contractions,,,,
3b73ee42-b00f-476e-a0ab-4e253b3f16c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3b73ee42-b00f-476e-a0ab-4e253b3f16c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3b73ee42-b00f-476e-a0ab-4e253b3f16c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3b73ee42-b00f-476e-a0ab-4e253b3f16c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3b73ee42-b00f-476e-a0ab-4e253b3f16c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3b73ee42-b00f-476e-a0ab-4e253b3f16c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3b73ee42-b00f-476e-a0ab-4e253b3f16c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3b73ee42-b00f-476e-a0ab-4e253b3f16c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3b73ee42-b00f-476e-a0ab-4e253b3f16c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3b73ee42-b00f-476e-a0ab-4e253b3f16c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3b73ee42-b00f-476e-a0ab-4e253b3f16c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3b73ee42-b00f-476e-a0ab-4e253b3f16c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3b73ee42-b00f-476e-a0ab-4e253b3f16c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3b73ee42-b00f-476e-a0ab-4e253b3f16c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3b73ee42-b00f-476e-a0ab-4e253b3f16c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3b73ee42-b00f-476e-a0ab-4e253b3f16c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3b73ee42-b00f-476e-a0ab-4e253b3f16c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
a5792f0d-d53a-4022-8d14-8d84a88deec6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Table 1.7: PVC summary.,True,Premature Ventricular Contractions,,,,
d1376cd8-d5c5-429e-b67c-967a2b14021c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Ventricular Tachycardia,False,Ventricular Tachycardia,,,,
d3f98d65-80d0-4548-9646-2e79d04744f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Ventricular tachycardia (VT) is caused by reentry currents being established in the ventricular myocardium or groups of ventricular myocytes that have aberrant electrical behavior. As such, VT is usually caused by underlying cardiac disease.",True,Ventricular Tachycardia,,,,
c3bd30b1-0e7e-4e84-9317-fa001e2b4aaf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Like a PVC, the aberrant depolarizations do not follow the normal conduction pathways so are wide (>120 msecs), but unlike a PVC, VT involves a ventricular rate >100 bpm. With disorganized contractility and reduced filling time, VT can lead to hemodynamic instability and severe hypotension—hence it is life threatening.",True,Ventricular Tachycardia,,,,
46d10fdd-b0f5-44bf-a0d6-46b0bb480f54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The QRS morphology in VT is highly variable between patients and depends on where the arrhythmia originates. Consequently there are several ways to classify VT based on duration, symptoms, QRS morphology, rate, and origin.",True,Ventricular Tachycardia,,,,
39ae95ea-9775-45df-8e9d-3290def46715,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Sustained VT is any VT that lasts for more than 30 seconds or is symptomatic. Nonsustained VT lasts for less than 30 seconds and is asymptomatic.,True,Ventricular Tachycardia,,,,
d909533e-2b33-428f-821c-f82bad4a0a08,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d909533e-2b33-428f-821c-f82bad4a0a08,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d909533e-2b33-428f-821c-f82bad4a0a08,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d909533e-2b33-428f-821c-f82bad4a0a08,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d909533e-2b33-428f-821c-f82bad4a0a08,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d909533e-2b33-428f-821c-f82bad4a0a08,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d909533e-2b33-428f-821c-f82bad4a0a08,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d909533e-2b33-428f-821c-f82bad4a0a08,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d909533e-2b33-428f-821c-f82bad4a0a08,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d909533e-2b33-428f-821c-f82bad4a0a08,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d909533e-2b33-428f-821c-f82bad4a0a08,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d909533e-2b33-428f-821c-f82bad4a0a08,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d909533e-2b33-428f-821c-f82bad4a0a08,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d909533e-2b33-428f-821c-f82bad4a0a08,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d909533e-2b33-428f-821c-f82bad4a0a08,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d909533e-2b33-428f-821c-f82bad4a0a08,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d909533e-2b33-428f-821c-f82bad4a0a08,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
dfffdbfb-f4ad-4039-891f-0198bf6112f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
dfffdbfb-f4ad-4039-891f-0198bf6112f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
dfffdbfb-f4ad-4039-891f-0198bf6112f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
dfffdbfb-f4ad-4039-891f-0198bf6112f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
dfffdbfb-f4ad-4039-891f-0198bf6112f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
dfffdbfb-f4ad-4039-891f-0198bf6112f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
dfffdbfb-f4ad-4039-891f-0198bf6112f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
dfffdbfb-f4ad-4039-891f-0198bf6112f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
dfffdbfb-f4ad-4039-891f-0198bf6112f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
dfffdbfb-f4ad-4039-891f-0198bf6112f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
dfffdbfb-f4ad-4039-891f-0198bf6112f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
dfffdbfb-f4ad-4039-891f-0198bf6112f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
dfffdbfb-f4ad-4039-891f-0198bf6112f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
dfffdbfb-f4ad-4039-891f-0198bf6112f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
dfffdbfb-f4ad-4039-891f-0198bf6112f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
dfffdbfb-f4ad-4039-891f-0198bf6112f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
dfffdbfb-f4ad-4039-891f-0198bf6112f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
d859396c-1f28-4cf7-9ff5-f6232712201f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Torsades de pointes is associated with a prolonged QT interval (>600 msecs) that helps distinguish it from other forms of polymorphous VT. The longer QT interval can be caused by ionic abnormalities that reduce the repolarizing current of Phase 3 of the cardiac action potential. This makes the myocardium susceptible to early after-depolarizations—the trigger for torsades de pointes. These after-depolarizations do not happen uniformly across the myocardium and are more common in endocardial tissue where the repolarization currents are slower. So torsades de pointes arises from the after-depolarizations causing reentry currents in neighboring tissue.,True,Ventricular Tachycardia,,,,
bbc3ab8a-b8f2-4a25-95a8-fe41db05a08b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Both common garden variety VTs and torsades de pointes can progress to ventricular fibrillation.,True,Ventricular Tachycardia,,,,
001252f6-7163-4758-8a8f-c42186806f4e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Table 1.8: VT summary.,True,Ventricular Tachycardia,,,,
c6cc99db-de1a-4e0c-90d6-36e3af13fa2a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Ventricular Fibrillation,False,Ventricular Fibrillation,,,,
344fd016-fbb6-4cdb-a1f2-865cfa6b6de9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Ventricular fibrillation (VF) occurs when the ventricular rate exceeds 400 bpm. The disorganized and uncoordinated contraction of the myocardium causes cardiac output to fall to catastrophic levels. Rates of survival for out-of-hospital VF are low.,True,Ventricular Fibrillation,,,,
fc249932-1c73-4ab7-a103-5e4252e1b58e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
fc249932-1c73-4ab7-a103-5e4252e1b58e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
fc249932-1c73-4ab7-a103-5e4252e1b58e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
fc249932-1c73-4ab7-a103-5e4252e1b58e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
fc249932-1c73-4ab7-a103-5e4252e1b58e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
fc249932-1c73-4ab7-a103-5e4252e1b58e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
fc249932-1c73-4ab7-a103-5e4252e1b58e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
fc249932-1c73-4ab7-a103-5e4252e1b58e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
fc249932-1c73-4ab7-a103-5e4252e1b58e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
fc249932-1c73-4ab7-a103-5e4252e1b58e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
fc249932-1c73-4ab7-a103-5e4252e1b58e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
fc249932-1c73-4ab7-a103-5e4252e1b58e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
fc249932-1c73-4ab7-a103-5e4252e1b58e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
fc249932-1c73-4ab7-a103-5e4252e1b58e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
fc249932-1c73-4ab7-a103-5e4252e1b58e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
fc249932-1c73-4ab7-a103-5e4252e1b58e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
fc249932-1c73-4ab7-a103-5e4252e1b58e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
28024bde-eda2-4dee-b9ac-37e887529c03,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Table 1.9: VF summary.,True,Ventricular Fibrillation,,,,
cd5c1383-7700-4e68-8859-044c267c0804,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,First-Degree Atrioventricular Block,False,First-Degree Atrioventricular Block,,,,
7fe8efe9-6fdf-4bae-9529-157321b9e80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
7fe8efe9-6fdf-4bae-9529-157321b9e80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
7fe8efe9-6fdf-4bae-9529-157321b9e80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
7fe8efe9-6fdf-4bae-9529-157321b9e80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
7fe8efe9-6fdf-4bae-9529-157321b9e80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
7fe8efe9-6fdf-4bae-9529-157321b9e80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
7fe8efe9-6fdf-4bae-9529-157321b9e80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
7fe8efe9-6fdf-4bae-9529-157321b9e80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
7fe8efe9-6fdf-4bae-9529-157321b9e80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
7fe8efe9-6fdf-4bae-9529-157321b9e80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
7fe8efe9-6fdf-4bae-9529-157321b9e80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
7fe8efe9-6fdf-4bae-9529-157321b9e80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
7fe8efe9-6fdf-4bae-9529-157321b9e80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
7fe8efe9-6fdf-4bae-9529-157321b9e80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
7fe8efe9-6fdf-4bae-9529-157321b9e80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
7fe8efe9-6fdf-4bae-9529-157321b9e80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
7fe8efe9-6fdf-4bae-9529-157321b9e80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ad9b2eaf-e5d7-4216-880d-3f1f42a36626,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ad9b2eaf-e5d7-4216-880d-3f1f42a36626,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ad9b2eaf-e5d7-4216-880d-3f1f42a36626,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ad9b2eaf-e5d7-4216-880d-3f1f42a36626,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ad9b2eaf-e5d7-4216-880d-3f1f42a36626,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ad9b2eaf-e5d7-4216-880d-3f1f42a36626,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ad9b2eaf-e5d7-4216-880d-3f1f42a36626,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ad9b2eaf-e5d7-4216-880d-3f1f42a36626,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ad9b2eaf-e5d7-4216-880d-3f1f42a36626,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ad9b2eaf-e5d7-4216-880d-3f1f42a36626,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ad9b2eaf-e5d7-4216-880d-3f1f42a36626,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ad9b2eaf-e5d7-4216-880d-3f1f42a36626,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ad9b2eaf-e5d7-4216-880d-3f1f42a36626,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ad9b2eaf-e5d7-4216-880d-3f1f42a36626,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ad9b2eaf-e5d7-4216-880d-3f1f42a36626,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ad9b2eaf-e5d7-4216-880d-3f1f42a36626,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ad9b2eaf-e5d7-4216-880d-3f1f42a36626,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
544d909a-de87-4311-acef-968d6b584902,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Table 1.10: First-degree block summary.,True,First-Degree Atrioventricular Block,,,,
a50f7806-9272-47d7-85a3-d4bcea316b8d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Second-Degree Atrioventricular Block,False,Second-Degree Atrioventricular Block,,,,
e757add6-b9fd-447b-9ade-719b7dc9066f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A second-degree atrioventricular block also has changes in P-R interval, but it starts to show failure of the P-wave to propagate a QRS complex every time (i.e., intermittently the depolarization fails to reach the ventricles). The pattern of missed ventricular depolarizations, or blocked P-waves, is often very regular and described as a ratio of P-waves to QRS complex. The way in which the P-R interval changes in relation to the blocked P-waves produces subclassifications of second-degree blocks, Mobitz I and II.",True,Second-Degree Atrioventricular Block,,,,
203a8b9e-dff0-4251-92d9-84e04e07f675,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
203a8b9e-dff0-4251-92d9-84e04e07f675,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
203a8b9e-dff0-4251-92d9-84e04e07f675,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
203a8b9e-dff0-4251-92d9-84e04e07f675,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
203a8b9e-dff0-4251-92d9-84e04e07f675,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
203a8b9e-dff0-4251-92d9-84e04e07f675,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
203a8b9e-dff0-4251-92d9-84e04e07f675,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
203a8b9e-dff0-4251-92d9-84e04e07f675,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
203a8b9e-dff0-4251-92d9-84e04e07f675,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
203a8b9e-dff0-4251-92d9-84e04e07f675,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
203a8b9e-dff0-4251-92d9-84e04e07f675,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
203a8b9e-dff0-4251-92d9-84e04e07f675,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
203a8b9e-dff0-4251-92d9-84e04e07f675,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
203a8b9e-dff0-4251-92d9-84e04e07f675,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
203a8b9e-dff0-4251-92d9-84e04e07f675,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
203a8b9e-dff0-4251-92d9-84e04e07f675,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
203a8b9e-dff0-4251-92d9-84e04e07f675,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
80d8b8ce-fd0b-4e3e-879b-20a11ca46183,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
80d8b8ce-fd0b-4e3e-879b-20a11ca46183,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
80d8b8ce-fd0b-4e3e-879b-20a11ca46183,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
80d8b8ce-fd0b-4e3e-879b-20a11ca46183,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
80d8b8ce-fd0b-4e3e-879b-20a11ca46183,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
80d8b8ce-fd0b-4e3e-879b-20a11ca46183,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
80d8b8ce-fd0b-4e3e-879b-20a11ca46183,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
80d8b8ce-fd0b-4e3e-879b-20a11ca46183,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
80d8b8ce-fd0b-4e3e-879b-20a11ca46183,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
80d8b8ce-fd0b-4e3e-879b-20a11ca46183,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
80d8b8ce-fd0b-4e3e-879b-20a11ca46183,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
80d8b8ce-fd0b-4e3e-879b-20a11ca46183,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
80d8b8ce-fd0b-4e3e-879b-20a11ca46183,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
80d8b8ce-fd0b-4e3e-879b-20a11ca46183,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
80d8b8ce-fd0b-4e3e-879b-20a11ca46183,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
80d8b8ce-fd0b-4e3e-879b-20a11ca46183,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
80d8b8ce-fd0b-4e3e-879b-20a11ca46183,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
0a42f511-a11f-44a8-9665-81661fd09ca2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Table 1.11: Second-degree block summary.,True,Second-Degree Atrioventricular Block,,,,
33723b6e-c661-4ab6-8565-a987cf260ce9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Third-Degree Atrioventricular Block,False,Third-Degree Atrioventricular Block,,,,
4d96c2f5-dda8-42d8-b90e-3c89b99d8bed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
4d96c2f5-dda8-42d8-b90e-3c89b99d8bed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
4d96c2f5-dda8-42d8-b90e-3c89b99d8bed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
4d96c2f5-dda8-42d8-b90e-3c89b99d8bed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
4d96c2f5-dda8-42d8-b90e-3c89b99d8bed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
4d96c2f5-dda8-42d8-b90e-3c89b99d8bed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
4d96c2f5-dda8-42d8-b90e-3c89b99d8bed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
4d96c2f5-dda8-42d8-b90e-3c89b99d8bed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
4d96c2f5-dda8-42d8-b90e-3c89b99d8bed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
4d96c2f5-dda8-42d8-b90e-3c89b99d8bed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
4d96c2f5-dda8-42d8-b90e-3c89b99d8bed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
4d96c2f5-dda8-42d8-b90e-3c89b99d8bed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
4d96c2f5-dda8-42d8-b90e-3c89b99d8bed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
4d96c2f5-dda8-42d8-b90e-3c89b99d8bed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
4d96c2f5-dda8-42d8-b90e-3c89b99d8bed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
4d96c2f5-dda8-42d8-b90e-3c89b99d8bed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
4d96c2f5-dda8-42d8-b90e-3c89b99d8bed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
45187700-21e0-4d7a-8bdb-6f090ad55154,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Table 1.12: Third-degree block summary.,True,Third-Degree Atrioventricular Block,,,,
0b228b18-9338-4fa3-ba07-ab675abdfe29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Left Bundle Branch Block,False,Left Bundle Branch Block,,,,
49cacec0-4e22-4e27-bd03-30c040c3c7b9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"A left bundle branch block (LBBB) is generated when the conductivity of the His-Purkinje system in the left ventricle is compromised, either through damage or disease. The ECG changes, and criteria for LBBB relate to these changes in conductivity and the left-side location.",True,Left Bundle Branch Block,,,,
ace660f0-1196-435e-b599-24dd45e756cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ace660f0-1196-435e-b599-24dd45e756cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ace660f0-1196-435e-b599-24dd45e756cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ace660f0-1196-435e-b599-24dd45e756cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ace660f0-1196-435e-b599-24dd45e756cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ace660f0-1196-435e-b599-24dd45e756cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ace660f0-1196-435e-b599-24dd45e756cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ace660f0-1196-435e-b599-24dd45e756cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ace660f0-1196-435e-b599-24dd45e756cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ace660f0-1196-435e-b599-24dd45e756cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ace660f0-1196-435e-b599-24dd45e756cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ace660f0-1196-435e-b599-24dd45e756cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ace660f0-1196-435e-b599-24dd45e756cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ace660f0-1196-435e-b599-24dd45e756cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ace660f0-1196-435e-b599-24dd45e756cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ace660f0-1196-435e-b599-24dd45e756cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ace660f0-1196-435e-b599-24dd45e756cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
efe3abd5-a0df-495e-89cf-bd173cbec475,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The lateral leads (I, V5, and V6) normally show a downward deflecting Q-wave as normal septal deflection initially occurs left-to-right (i.e., away from the lateral leads). In LBBB the change in direction to right-to-left, plus the longer duration, eliminates the Q-wave from the lateral leads, and Q-waves will be small in aVL.",True,Left Bundle Branch Block,,,,
9ab0ed33-e161-40d9-b5d5-301db52f93d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
9ab0ed33-e161-40d9-b5d5-301db52f93d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
9ab0ed33-e161-40d9-b5d5-301db52f93d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
9ab0ed33-e161-40d9-b5d5-301db52f93d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
9ab0ed33-e161-40d9-b5d5-301db52f93d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
9ab0ed33-e161-40d9-b5d5-301db52f93d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
9ab0ed33-e161-40d9-b5d5-301db52f93d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
9ab0ed33-e161-40d9-b5d5-301db52f93d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
9ab0ed33-e161-40d9-b5d5-301db52f93d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
9ab0ed33-e161-40d9-b5d5-301db52f93d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
9ab0ed33-e161-40d9-b5d5-301db52f93d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
9ab0ed33-e161-40d9-b5d5-301db52f93d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
9ab0ed33-e161-40d9-b5d5-301db52f93d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
9ab0ed33-e161-40d9-b5d5-301db52f93d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
9ab0ed33-e161-40d9-b5d5-301db52f93d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
9ab0ed33-e161-40d9-b5d5-301db52f93d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
9ab0ed33-e161-40d9-b5d5-301db52f93d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
925defca-14de-4a6f-9cef-e505534719d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
925defca-14de-4a6f-9cef-e505534719d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
925defca-14de-4a6f-9cef-e505534719d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
925defca-14de-4a6f-9cef-e505534719d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
925defca-14de-4a6f-9cef-e505534719d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
925defca-14de-4a6f-9cef-e505534719d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
925defca-14de-4a6f-9cef-e505534719d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
925defca-14de-4a6f-9cef-e505534719d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
925defca-14de-4a6f-9cef-e505534719d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
925defca-14de-4a6f-9cef-e505534719d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
925defca-14de-4a6f-9cef-e505534719d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
925defca-14de-4a6f-9cef-e505534719d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
925defca-14de-4a6f-9cef-e505534719d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
925defca-14de-4a6f-9cef-e505534719d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
925defca-14de-4a6f-9cef-e505534719d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
925defca-14de-4a6f-9cef-e505534719d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
925defca-14de-4a6f-9cef-e505534719d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
735d7e6d-753c-498a-ace3-03aa584a4c51,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Table 1.13: LBBB summary.,True,Left Bundle Branch Block,,,,
a5da6b72-ab71-41c6-b390-24ac3d1b5fa3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Right Bundle Branch Block,False,Right Bundle Branch Block,,,,
c1f9dfeb-12e8-4bb3-81db-0a4dfa124911,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The causes and manifestations of a right bundle branch block (RBBB) bear some similarities to those described for LBBB, but of course this time its depolarization of the right ventricle is delayed. Causes of RBBB include ischemic heart disease again as well as other myocardial diseases, but pulmonary issues such as pulmonary embolism and cor pulmonale can be added to the list.",True,Right Bundle Branch Block,,,,
80fcd71e-9489-4bba-bc19-54fcd9f9e79e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
80fcd71e-9489-4bba-bc19-54fcd9f9e79e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
80fcd71e-9489-4bba-bc19-54fcd9f9e79e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
80fcd71e-9489-4bba-bc19-54fcd9f9e79e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
80fcd71e-9489-4bba-bc19-54fcd9f9e79e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
80fcd71e-9489-4bba-bc19-54fcd9f9e79e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
80fcd71e-9489-4bba-bc19-54fcd9f9e79e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
80fcd71e-9489-4bba-bc19-54fcd9f9e79e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
80fcd71e-9489-4bba-bc19-54fcd9f9e79e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
80fcd71e-9489-4bba-bc19-54fcd9f9e79e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
80fcd71e-9489-4bba-bc19-54fcd9f9e79e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
80fcd71e-9489-4bba-bc19-54fcd9f9e79e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
80fcd71e-9489-4bba-bc19-54fcd9f9e79e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
80fcd71e-9489-4bba-bc19-54fcd9f9e79e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
80fcd71e-9489-4bba-bc19-54fcd9f9e79e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
80fcd71e-9489-4bba-bc19-54fcd9f9e79e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
80fcd71e-9489-4bba-bc19-54fcd9f9e79e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
8216e26a-ef61-4c36-aafc-9275edbf22e8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Table 1.14: RBBB summary.,True,Right Bundle Branch Block,,,,
c0f9b68d-d49d-4369-9bf6-8520147fb73f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Wolff-Parkinson-White Syndrome,False,Wolff-Parkinson-White Syndrome,,,,
c16cfe08-a1ab-48fb-baeb-8a0a3107d7c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Normally the only electrical connection between the atria and the ventricles is the AV node. Otherwise the fibrous skeleton of the heart electrically insulates the atria from the ventricles. In Wolff-Parkinson-White (WPW) syndrome, that insulation is incomplete, and an “accessory pathway” connects the electrical system of the atria directly to the ventricles. If you think of the AV node as a bridge over the fibrous wall with regulated access, the accessory pathway is like a pathological tunnel under it with no regulation.",True,Wolff-Parkinson-White Syndrome,,,,
c1b446cb-1ac9-4c44-8a03-535ad8c32027,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c1b446cb-1ac9-4c44-8a03-535ad8c32027,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c1b446cb-1ac9-4c44-8a03-535ad8c32027,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c1b446cb-1ac9-4c44-8a03-535ad8c32027,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c1b446cb-1ac9-4c44-8a03-535ad8c32027,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c1b446cb-1ac9-4c44-8a03-535ad8c32027,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c1b446cb-1ac9-4c44-8a03-535ad8c32027,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c1b446cb-1ac9-4c44-8a03-535ad8c32027,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c1b446cb-1ac9-4c44-8a03-535ad8c32027,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c1b446cb-1ac9-4c44-8a03-535ad8c32027,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c1b446cb-1ac9-4c44-8a03-535ad8c32027,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c1b446cb-1ac9-4c44-8a03-535ad8c32027,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c1b446cb-1ac9-4c44-8a03-535ad8c32027,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c1b446cb-1ac9-4c44-8a03-535ad8c32027,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c1b446cb-1ac9-4c44-8a03-535ad8c32027,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c1b446cb-1ac9-4c44-8a03-535ad8c32027,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c1b446cb-1ac9-4c44-8a03-535ad8c32027,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
164325c4-5e47-4657-a025-44eb683f122c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"WPW syndrome is often asymptomatic, and patients do not require immediate treatment. However, if atrial fibrillation occurs in a WPW patient, the accessory pathway can allow the atrial fibrillation waves through to the ventricle (with no AV nodal refractory period to prevent them). Consequently a high ventricular rate is seen, and the risk of ventricular fibrillation being established means immediate clinical attention is required.",True,Wolff-Parkinson-White Syndrome,,,,
1fae8870-88b0-449a-b76f-9ccfa68792d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Hyper- and Hypocalcemia,False,Hyper- and Hypocalcemia,,,,
d72ea970-f8d7-4da1-9dcd-89e9e5cc8e7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
d72ea970-f8d7-4da1-9dcd-89e9e5cc8e7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
d72ea970-f8d7-4da1-9dcd-89e9e5cc8e7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
d72ea970-f8d7-4da1-9dcd-89e9e5cc8e7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
d72ea970-f8d7-4da1-9dcd-89e9e5cc8e7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
d72ea970-f8d7-4da1-9dcd-89e9e5cc8e7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
d72ea970-f8d7-4da1-9dcd-89e9e5cc8e7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
d72ea970-f8d7-4da1-9dcd-89e9e5cc8e7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
d72ea970-f8d7-4da1-9dcd-89e9e5cc8e7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
d72ea970-f8d7-4da1-9dcd-89e9e5cc8e7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
d72ea970-f8d7-4da1-9dcd-89e9e5cc8e7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
d72ea970-f8d7-4da1-9dcd-89e9e5cc8e7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
d72ea970-f8d7-4da1-9dcd-89e9e5cc8e7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
d72ea970-f8d7-4da1-9dcd-89e9e5cc8e7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
d72ea970-f8d7-4da1-9dcd-89e9e5cc8e7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
d72ea970-f8d7-4da1-9dcd-89e9e5cc8e7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
d72ea970-f8d7-4da1-9dcd-89e9e5cc8e7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
0286520b-9baa-4884-9518-fc695d966316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
0286520b-9baa-4884-9518-fc695d966316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
0286520b-9baa-4884-9518-fc695d966316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
0286520b-9baa-4884-9518-fc695d966316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
0286520b-9baa-4884-9518-fc695d966316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
0286520b-9baa-4884-9518-fc695d966316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
0286520b-9baa-4884-9518-fc695d966316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
0286520b-9baa-4884-9518-fc695d966316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
0286520b-9baa-4884-9518-fc695d966316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
0286520b-9baa-4884-9518-fc695d966316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
0286520b-9baa-4884-9518-fc695d966316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
0286520b-9baa-4884-9518-fc695d966316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
0286520b-9baa-4884-9518-fc695d966316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
0286520b-9baa-4884-9518-fc695d966316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
0286520b-9baa-4884-9518-fc695d966316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
0286520b-9baa-4884-9518-fc695d966316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
0286520b-9baa-4884-9518-fc695d966316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
29e51c74-af0f-4efd-bc86-0ca98258aea6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Table 1.16: Hyper- and hypocalcemia summary.,True,Hyper- and Hypocalcemia,,,,
baddbda7-9fc3-4d21-adee-5c3f6e4e674e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Hyper- and Hypokalemia,False,Hyper- and Hypokalemia,,,,
4cb1a075-cdf8-4a84-9c74-571360e12233,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"The pathophysiology is not as simple as changes in extracellular K+ changing the electrochemical gradient for K+. Because of potassium’s role in maintaining the resting membrane potential, shifts in extracellular potassium can also influence the activity of Na+ and Ca++ channels.",True,Hyper- and Hypokalemia,,,,
1f332180-aedf-47eb-a5a7-a801770dbfe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
1f332180-aedf-47eb-a5a7-a801770dbfe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
1f332180-aedf-47eb-a5a7-a801770dbfe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
1f332180-aedf-47eb-a5a7-a801770dbfe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
1f332180-aedf-47eb-a5a7-a801770dbfe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
1f332180-aedf-47eb-a5a7-a801770dbfe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
1f332180-aedf-47eb-a5a7-a801770dbfe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
1f332180-aedf-47eb-a5a7-a801770dbfe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
1f332180-aedf-47eb-a5a7-a801770dbfe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
1f332180-aedf-47eb-a5a7-a801770dbfe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
1f332180-aedf-47eb-a5a7-a801770dbfe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
1f332180-aedf-47eb-a5a7-a801770dbfe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
1f332180-aedf-47eb-a5a7-a801770dbfe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
1f332180-aedf-47eb-a5a7-a801770dbfe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
1f332180-aedf-47eb-a5a7-a801770dbfe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
1f332180-aedf-47eb-a5a7-a801770dbfe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
1f332180-aedf-47eb-a5a7-a801770dbfe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
3164724b-5a0e-49de-87fb-c01a532ae57b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"As hypokalemia also inhibits Na+-K+ ATPase, Na+ accumulates inside the cell. This in turn leads to an accumulation of Ca++ because of a subsequent failure of the Na+-Ca++ exchanger. Extended presence of these two positive ions inside the myocyte prolongs the action potential and may manifest as an increased width and amplitude of the P-wave.",True,Hyper- and Hypokalemia,,,,
52bce982-7be6-45c7-b379-20159ca2f099,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"As hypokalemia worsens, the problems with K+ conductance and repolarization increase, and the myocardium becomes susceptible to early after-depolarization (EAD) arrhythmias.",True,Hyper- and Hypokalemia,,,,
7b78490d-2ce3-4251-aef1-703c63a8835c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
7b78490d-2ce3-4251-aef1-703c63a8835c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
7b78490d-2ce3-4251-aef1-703c63a8835c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
7b78490d-2ce3-4251-aef1-703c63a8835c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
7b78490d-2ce3-4251-aef1-703c63a8835c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
7b78490d-2ce3-4251-aef1-703c63a8835c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
7b78490d-2ce3-4251-aef1-703c63a8835c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
7b78490d-2ce3-4251-aef1-703c63a8835c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
7b78490d-2ce3-4251-aef1-703c63a8835c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
7b78490d-2ce3-4251-aef1-703c63a8835c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
7b78490d-2ce3-4251-aef1-703c63a8835c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
7b78490d-2ce3-4251-aef1-703c63a8835c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
7b78490d-2ce3-4251-aef1-703c63a8835c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
7b78490d-2ce3-4251-aef1-703c63a8835c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
7b78490d-2ce3-4251-aef1-703c63a8835c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
7b78490d-2ce3-4251-aef1-703c63a8835c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
7b78490d-2ce3-4251-aef1-703c63a8835c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
e3ea0661-4819-4ae9-a476-d67adf66393f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
e3ea0661-4819-4ae9-a476-d67adf66393f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
e3ea0661-4819-4ae9-a476-d67adf66393f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
e3ea0661-4819-4ae9-a476-d67adf66393f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
e3ea0661-4819-4ae9-a476-d67adf66393f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
e3ea0661-4819-4ae9-a476-d67adf66393f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
e3ea0661-4819-4ae9-a476-d67adf66393f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
e3ea0661-4819-4ae9-a476-d67adf66393f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
e3ea0661-4819-4ae9-a476-d67adf66393f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
e3ea0661-4819-4ae9-a476-d67adf66393f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
e3ea0661-4819-4ae9-a476-d67adf66393f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
e3ea0661-4819-4ae9-a476-d67adf66393f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
e3ea0661-4819-4ae9-a476-d67adf66393f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
e3ea0661-4819-4ae9-a476-d67adf66393f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
e3ea0661-4819-4ae9-a476-d67adf66393f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
e3ea0661-4819-4ae9-a476-d67adf66393f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
e3ea0661-4819-4ae9-a476-d67adf66393f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
73e4f4a1-15a8-4f0a-9d3f-db1a4c1b823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
73e4f4a1-15a8-4f0a-9d3f-db1a4c1b823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
73e4f4a1-15a8-4f0a-9d3f-db1a4c1b823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
73e4f4a1-15a8-4f0a-9d3f-db1a4c1b823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
73e4f4a1-15a8-4f0a-9d3f-db1a4c1b823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
73e4f4a1-15a8-4f0a-9d3f-db1a4c1b823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
73e4f4a1-15a8-4f0a-9d3f-db1a4c1b823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
73e4f4a1-15a8-4f0a-9d3f-db1a4c1b823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
73e4f4a1-15a8-4f0a-9d3f-db1a4c1b823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
73e4f4a1-15a8-4f0a-9d3f-db1a4c1b823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
73e4f4a1-15a8-4f0a-9d3f-db1a4c1b823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
73e4f4a1-15a8-4f0a-9d3f-db1a4c1b823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
73e4f4a1-15a8-4f0a-9d3f-db1a4c1b823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
73e4f4a1-15a8-4f0a-9d3f-db1a4c1b823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
73e4f4a1-15a8-4f0a-9d3f-db1a4c1b823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
73e4f4a1-15a8-4f0a-9d3f-db1a4c1b823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
73e4f4a1-15a8-4f0a-9d3f-db1a4c1b823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
fc40bad3-63fd-44a7-a624-75b1604eab33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fc40bad3-63fd-44a7-a624-75b1604eab33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fc40bad3-63fd-44a7-a624-75b1604eab33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fc40bad3-63fd-44a7-a624-75b1604eab33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fc40bad3-63fd-44a7-a624-75b1604eab33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fc40bad3-63fd-44a7-a624-75b1604eab33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fc40bad3-63fd-44a7-a624-75b1604eab33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fc40bad3-63fd-44a7-a624-75b1604eab33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fc40bad3-63fd-44a7-a624-75b1604eab33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fc40bad3-63fd-44a7-a624-75b1604eab33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fc40bad3-63fd-44a7-a624-75b1604eab33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fc40bad3-63fd-44a7-a624-75b1604eab33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fc40bad3-63fd-44a7-a624-75b1604eab33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fc40bad3-63fd-44a7-a624-75b1604eab33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fc40bad3-63fd-44a7-a624-75b1604eab33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fc40bad3-63fd-44a7-a624-75b1604eab33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fc40bad3-63fd-44a7-a624-75b1604eab33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
83d9472e-e051-44ef-98b0-28a906aa7205,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Table 1.17: Hypo- and hyperkalemia summary.,True,Hyper- and Hypokalemia,,,,
70920070-50d7-444c-bfde-aa691d4e710a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"References, resources, and further reading",False,"References, resources, and further reading",,,,
18b18aec-7be2-4f27-a784-332ad57a235f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,Text,False,Text,,,,
408d33e2-8cd9-4ec0-8987-20e9971994dd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Burns, Ed, and Robert Buttner. Hypercalcaemia. Lift in the Fast Lane, 2021. https://litfl.com/hypercalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
37dd5fd7-9e0e-40f8-b46c-cb4809eb62a2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Burns, Ed, and Robert Buttner. Hypocalcaemia. Life in the Fast Lane, 2021. https://litfl.com/hypocalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
1c3aef94-bfae-49c7-9f3c-de8c9cf7d8eb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Buttner, Robert, and Ed Burns. Hyperkalaemia. Life in the Fast Lane. https://litfl.com/hyperkalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
11235949-0c37-4fcc-86c9-3fea7130d670,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Buttner, Robert, and Ed Burns. Hypokalaemia. Life in the Fast Lane, 2021. https://litfl.com/hypokalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
3ec23555-9a99-4afe-949b-9e0d4d06a8d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Chhabra, Lovely, Amandeep Goyal, and Michael D. Benham. Wolff Parkinson White Syndrome. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK554437/, CC BY 4.0.",True,Text,,,,
9cdb6710-410a-4e66-843f-d613206b5333,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Custer, Adam M., Varun S. Yelamanchili, and Sarah L. Lappin. Multifocal Atrial Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459152/, CC BY 4.0.",True,Text,,,,
71747b14-7fe0-4733-8028-1c9d310f130b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Farzam, Khashayar, and John R. Richards. Premature Ventricular Contraction. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532991/, CC BY 4.0.",True,Text,,,,
b9dbddff-1f83-4981-9737-c5a42e77e71f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Foth, Christopher, Manesh Kumar Gangwani, and Heidi Alvey. Ventricular Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532954/, CC BY 4.0.",True,Text,,,,
3b935a35-6c3e-4727-a0b6-bab392a1e27e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Hafeez, Yamama, and Shamai A. Grossman. Sinus Bradycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK493201/, CC BY 4.0.",True,Text,,,,
a07e9af8-6a7e-42c2-a3cf-a8134abd0947,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Harkness, Weston T., and Mary Hicks. Right Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK507872/, CC BY 4.0.",True,Text,,,,
8716fa6a-ec60-43ee-985d-ca89b967c718,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Heaton, Joseph, and Srikanth Yandrapalli. Premature Atrial Contractions. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK559204/, CC BY 4.0.",True,Text,,,,
c288acf2-eda2-4cd4-8039-2a14e49a4ae7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Kashou, Anthony H., Amandeep Goyal, Tran Nguyen, and Lovely Chhabra. Atrioventricular Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459147/, CC BY 4.0.",True,Text,,,,
fc14e3b5-823d-41e6-87c9-7d4ce891fcbf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,“Learn the Heart.” Healio. https://www.healio.com/cardiology/learn-the-heart.,True,Text,,,,
b860757d-f7ba-4f6e-80ea-1b8b63f906ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Ludhwani, Dipesh, Amandeep Goyal, and Mandar Jagtap. Ventricular Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK537120/, CC BY 4.0.",True,Text,,,,
e57ae199-bc34-48b0-8bb3-5e8bb0f93cc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Nesheiwat, Zeid, Amandeep Goyal, and Mandar Jagtap. Atrial Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK526072/, CC BY 4.0.",True,Text,,,,
30a9df7c-0357-4037-9d56-c7d4765f8a62,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Pipilas, Daniel C., Bruce A. Koplan, and Leonard S. Lilly. “The Electrocardiogram.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 4. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
16092a29-0f0c-45dd-8485-dd7e84788a20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Rodriguez Ziccardi, Mary, Amandeep Goyal, and Christopher V. Maani. Atrial Flutter. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK540985/, CC BY 4.0.",True,Text,,,,
96a78e09-43e0-4862-a9c8-efffad490150,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-12,"Scherbak, Dmitriy, and Gregory J. Hicks. Left Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK482167/, CC BY 4.0.",True,Text,,,,
b0a38261-1ed4-4c9d-b130-8d5a9d09acd0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,USMLE,False,USMLE,,,,
76a7b7d6-6642-48e6-a0c5-2c1f29b6df57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
76a7b7d6-6642-48e6-a0c5-2c1f29b6df57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
76a7b7d6-6642-48e6-a0c5-2c1f29b6df57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
76a7b7d6-6642-48e6-a0c5-2c1f29b6df57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
76a7b7d6-6642-48e6-a0c5-2c1f29b6df57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
76a7b7d6-6642-48e6-a0c5-2c1f29b6df57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
76a7b7d6-6642-48e6-a0c5-2c1f29b6df57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
76a7b7d6-6642-48e6-a0c5-2c1f29b6df57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
76a7b7d6-6642-48e6-a0c5-2c1f29b6df57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
76a7b7d6-6642-48e6-a0c5-2c1f29b6df57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
76a7b7d6-6642-48e6-a0c5-2c1f29b6df57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
76a7b7d6-6642-48e6-a0c5-2c1f29b6df57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
76a7b7d6-6642-48e6-a0c5-2c1f29b6df57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
76a7b7d6-6642-48e6-a0c5-2c1f29b6df57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
76a7b7d6-6642-48e6-a0c5-2c1f29b6df57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
76a7b7d6-6642-48e6-a0c5-2c1f29b6df57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
76a7b7d6-6642-48e6-a0c5-2c1f29b6df57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
1364eec2-f30b-4197-ae35-89a12d011979,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,10q22,False,10q22,,,,
b0e9f4dc-2c31-4b4f-94a9-6af4abb1683d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,q24,False,q24,,,,
6444462e-15bb-454d-a0d0-b2eff731b8ef,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,fibrillatory,False,fibrillatory,,,,
601df554-b535-4dc8-bbee-3d4100e0857e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
601df554-b535-4dc8-bbee-3d4100e0857e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
601df554-b535-4dc8-bbee-3d4100e0857e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
601df554-b535-4dc8-bbee-3d4100e0857e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
601df554-b535-4dc8-bbee-3d4100e0857e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
601df554-b535-4dc8-bbee-3d4100e0857e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
601df554-b535-4dc8-bbee-3d4100e0857e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
601df554-b535-4dc8-bbee-3d4100e0857e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
601df554-b535-4dc8-bbee-3d4100e0857e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
601df554-b535-4dc8-bbee-3d4100e0857e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
601df554-b535-4dc8-bbee-3d4100e0857e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
601df554-b535-4dc8-bbee-3d4100e0857e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
601df554-b535-4dc8-bbee-3d4100e0857e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
601df554-b535-4dc8-bbee-3d4100e0857e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
601df554-b535-4dc8-bbee-3d4100e0857e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
601df554-b535-4dc8-bbee-3d4100e0857e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
601df554-b535-4dc8-bbee-3d4100e0857e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d3edd7ca-69b0-4bad-a734-507c978452d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Table 1.1: Atrial fibrillation summary.,True,fibrillatory,,,,
33762aba-fe5f-448d-9ce7-df229137510e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Atrial Flutter,False,Atrial Flutter,,,,
978dd31b-fae0-48dd-bc7a-b1d999b5cfb3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
978dd31b-fae0-48dd-bc7a-b1d999b5cfb3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
978dd31b-fae0-48dd-bc7a-b1d999b5cfb3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
978dd31b-fae0-48dd-bc7a-b1d999b5cfb3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
978dd31b-fae0-48dd-bc7a-b1d999b5cfb3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
978dd31b-fae0-48dd-bc7a-b1d999b5cfb3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
978dd31b-fae0-48dd-bc7a-b1d999b5cfb3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
978dd31b-fae0-48dd-bc7a-b1d999b5cfb3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
978dd31b-fae0-48dd-bc7a-b1d999b5cfb3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
978dd31b-fae0-48dd-bc7a-b1d999b5cfb3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
978dd31b-fae0-48dd-bc7a-b1d999b5cfb3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
978dd31b-fae0-48dd-bc7a-b1d999b5cfb3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
978dd31b-fae0-48dd-bc7a-b1d999b5cfb3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
978dd31b-fae0-48dd-bc7a-b1d999b5cfb3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
978dd31b-fae0-48dd-bc7a-b1d999b5cfb3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
978dd31b-fae0-48dd-bc7a-b1d999b5cfb3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
978dd31b-fae0-48dd-bc7a-b1d999b5cfb3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
c2f1755b-4b1f-4a35-9686-0bb17b31327e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,macroreentrant,False,macroreentrant,,,,
c4a5cab7-a6de-40b7-98bb-b338cbd0edbb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,cavotricuspid,False,cavotricuspid,,,,
66f99d21-d635-422d-9aae-d06ccf0d1d4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"As with atrial fibrillation, the AV node’s refractory period prevents most of the P-waves from progressing to the ventricle, but commonly the AV conduction will be 2-to-1, so with an atrial rate of 300 bpm the ventricular rate will be 150 bpm. Parasympathetic stimulation or changes in AV node refractoriness can modify how many P-waves pass into the ventricle, but the the resultant rhythm is “regularly irregular.” When the heart rate is elevated, then distinguishing flutter from fibrillation becomes challenging and slowing ventricular rate pharmaceutically (adenosine) helps the flutter waves reemerge for a definitive diagnosis to be made.",True,cavotricuspid,,,,
a65f9b49-8bb8-4207-8fa6-fcd397984437,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Table 1.2: Atrial flutter summary.,True,cavotricuspid,,,,
5663dbd8-0d32-4ea9-8346-5dcd5ff431e5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Multifocal Atrial Tachycardia,False,Multifocal Atrial Tachycardia,,,,
5914aa4a-237d-415c-8eb4-c24f9db920d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
5914aa4a-237d-415c-8eb4-c24f9db920d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
5914aa4a-237d-415c-8eb4-c24f9db920d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
5914aa4a-237d-415c-8eb4-c24f9db920d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
5914aa4a-237d-415c-8eb4-c24f9db920d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
5914aa4a-237d-415c-8eb4-c24f9db920d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
5914aa4a-237d-415c-8eb4-c24f9db920d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
5914aa4a-237d-415c-8eb4-c24f9db920d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
5914aa4a-237d-415c-8eb4-c24f9db920d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
5914aa4a-237d-415c-8eb4-c24f9db920d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
5914aa4a-237d-415c-8eb4-c24f9db920d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
5914aa4a-237d-415c-8eb4-c24f9db920d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
5914aa4a-237d-415c-8eb4-c24f9db920d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
5914aa4a-237d-415c-8eb4-c24f9db920d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
5914aa4a-237d-415c-8eb4-c24f9db920d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
5914aa4a-237d-415c-8eb4-c24f9db920d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
5914aa4a-237d-415c-8eb4-c24f9db920d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
d5d9e75c-9db2-44ca-80e1-e4c3393be165,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"MAT frequently occurs in the setting of severe lung disease and, more specifically, during an exacerbation of lung disease. This rhythm is benign, and once the underlying lung disease is treated, it should resolve.",True,Multifocal Atrial Tachycardia,,,,
7ed99e6d-108d-4f0b-a028-a52d5944a923,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Table 1.3: MAT summary.,True,Multifocal Atrial Tachycardia,,,,
1b905d21-4663-48e3-88f6-4ee308457a30,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Premature Atrial Contraction,False,Premature Atrial Contraction,,,,
8de3c409-f963-4352-8421-54dcaa8ea6d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A premature atrial contraction (PAC) is generated by a depolarization instigated outside of the SA node. This produces an extra P-wave, and consequently a shortening from previous P-P intervals is seen. The aberrant P-wave also has a different morphology from a sinus P-wave because of its different anatomical origin.",True,Premature Atrial Contraction,,,,
606337a7-53e7-47bc-9e4e-bc903d21fbb7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
606337a7-53e7-47bc-9e4e-bc903d21fbb7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
606337a7-53e7-47bc-9e4e-bc903d21fbb7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
606337a7-53e7-47bc-9e4e-bc903d21fbb7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
606337a7-53e7-47bc-9e4e-bc903d21fbb7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
606337a7-53e7-47bc-9e4e-bc903d21fbb7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
606337a7-53e7-47bc-9e4e-bc903d21fbb7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
606337a7-53e7-47bc-9e4e-bc903d21fbb7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
606337a7-53e7-47bc-9e4e-bc903d21fbb7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
606337a7-53e7-47bc-9e4e-bc903d21fbb7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
606337a7-53e7-47bc-9e4e-bc903d21fbb7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
606337a7-53e7-47bc-9e4e-bc903d21fbb7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
606337a7-53e7-47bc-9e4e-bc903d21fbb7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
606337a7-53e7-47bc-9e4e-bc903d21fbb7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
606337a7-53e7-47bc-9e4e-bc903d21fbb7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
606337a7-53e7-47bc-9e4e-bc903d21fbb7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
606337a7-53e7-47bc-9e4e-bc903d21fbb7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
cc6dc371-7526-42fe-a3d4-7c88b502565d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"If a PAC occurs when the AV node has not yet recovered from its refractory period, the PAC will fail to conduct to the ventricles; meaning the PAC will not be followed by a QRS complex or the ectopic P-R interval will be prolonged. The ECG will show a premature, ectopic P-wave and then no QRS complex afterward. When this occurs along with bigeminy, the ECG can appear as if there is sinus bradycardia.",True,Premature Atrial Contraction,,,,
0e3dbcf0-9b40-4fc2-a672-81efeb2a7cb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Table 1.4: PAC summary.,True,Premature Atrial Contraction,,,,
e2655b6f-f3a4-455c-9683-9a9724a5c630,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Sinus Bradycardia,False,Sinus Bradycardia,,,,
e1b5141a-85df-4c4b-afd4-3d9411ef3412,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Sinus bradycardia denotes a sinus rhythm below 60 bpm. Otherwise the ECG waveform is normal on an ECG with an upright P-wave in lead II preceding every QRS complex. There are many intrinsic causes associated with the heart itself, as well as extrinsic causes, some of which are listed table 1.5. Sinus bradycardia is usually asymptomatic as rates of 40–50 bpm can maintain hemodynamic stability. Rates below this can produce symptoms of fatigue, dizziness, and dyspnea on exertion.",True,Sinus Bradycardia,,,,
dcca14b6-5cac-4767-b632-2fa7fafeff8d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Table 1.5: Intrinsic and extrinsic causes associated with the heart.,True,Sinus Bradycardia,,,,
37a2585a-344f-4675-872e-d76c7ebc6b53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Table 1.6: Sinus bradycardia summary.,True,Sinus Bradycardia,,,,
d3647721-9135-4779-a8b1-f7656865a029,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Premature Ventricular Contractions,False,Premature Ventricular Contractions,,,,
3e9bd701-43c6-4dc1-8d12-eb6bf35a5c01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e9bd701-43c6-4dc1-8d12-eb6bf35a5c01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e9bd701-43c6-4dc1-8d12-eb6bf35a5c01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e9bd701-43c6-4dc1-8d12-eb6bf35a5c01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e9bd701-43c6-4dc1-8d12-eb6bf35a5c01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e9bd701-43c6-4dc1-8d12-eb6bf35a5c01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e9bd701-43c6-4dc1-8d12-eb6bf35a5c01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e9bd701-43c6-4dc1-8d12-eb6bf35a5c01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e9bd701-43c6-4dc1-8d12-eb6bf35a5c01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e9bd701-43c6-4dc1-8d12-eb6bf35a5c01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e9bd701-43c6-4dc1-8d12-eb6bf35a5c01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e9bd701-43c6-4dc1-8d12-eb6bf35a5c01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e9bd701-43c6-4dc1-8d12-eb6bf35a5c01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e9bd701-43c6-4dc1-8d12-eb6bf35a5c01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e9bd701-43c6-4dc1-8d12-eb6bf35a5c01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e9bd701-43c6-4dc1-8d12-eb6bf35a5c01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e9bd701-43c6-4dc1-8d12-eb6bf35a5c01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
c2d831de-0dbb-408f-8816-1a1526c37f95,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Table 1.7: PVC summary.,True,Premature Ventricular Contractions,,,,
8d690aae-7f80-4892-a081-cb6ea471c7d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Ventricular Tachycardia,False,Ventricular Tachycardia,,,,
daf1b8ff-348b-4b96-b56c-154203b36ea4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Ventricular tachycardia (VT) is caused by reentry currents being established in the ventricular myocardium or groups of ventricular myocytes that have aberrant electrical behavior. As such, VT is usually caused by underlying cardiac disease.",True,Ventricular Tachycardia,,,,
9339ed50-060f-4047-9458-7f70ba44d19d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Like a PVC, the aberrant depolarizations do not follow the normal conduction pathways so are wide (>120 msecs), but unlike a PVC, VT involves a ventricular rate >100 bpm. With disorganized contractility and reduced filling time, VT can lead to hemodynamic instability and severe hypotension—hence it is life threatening.",True,Ventricular Tachycardia,,,,
f655dc92-2d33-4685-a2cf-8f683e61a9c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The QRS morphology in VT is highly variable between patients and depends on where the arrhythmia originates. Consequently there are several ways to classify VT based on duration, symptoms, QRS morphology, rate, and origin.",True,Ventricular Tachycardia,,,,
70bbacd8-29cf-4a5b-960f-fe9e33ac3548,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Sustained VT is any VT that lasts for more than 30 seconds or is symptomatic. Nonsustained VT lasts for less than 30 seconds and is asymptomatic.,True,Ventricular Tachycardia,,,,
df5bc1f2-f052-4baa-a471-11de56c39b67,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
df5bc1f2-f052-4baa-a471-11de56c39b67,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
df5bc1f2-f052-4baa-a471-11de56c39b67,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
df5bc1f2-f052-4baa-a471-11de56c39b67,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
df5bc1f2-f052-4baa-a471-11de56c39b67,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
df5bc1f2-f052-4baa-a471-11de56c39b67,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
df5bc1f2-f052-4baa-a471-11de56c39b67,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
df5bc1f2-f052-4baa-a471-11de56c39b67,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
df5bc1f2-f052-4baa-a471-11de56c39b67,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
df5bc1f2-f052-4baa-a471-11de56c39b67,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
df5bc1f2-f052-4baa-a471-11de56c39b67,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
df5bc1f2-f052-4baa-a471-11de56c39b67,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
df5bc1f2-f052-4baa-a471-11de56c39b67,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
df5bc1f2-f052-4baa-a471-11de56c39b67,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
df5bc1f2-f052-4baa-a471-11de56c39b67,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
df5bc1f2-f052-4baa-a471-11de56c39b67,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
df5bc1f2-f052-4baa-a471-11de56c39b67,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
9ba5b5dc-ddd1-425d-94f7-17d3beddc0fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
9ba5b5dc-ddd1-425d-94f7-17d3beddc0fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
9ba5b5dc-ddd1-425d-94f7-17d3beddc0fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
9ba5b5dc-ddd1-425d-94f7-17d3beddc0fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
9ba5b5dc-ddd1-425d-94f7-17d3beddc0fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
9ba5b5dc-ddd1-425d-94f7-17d3beddc0fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
9ba5b5dc-ddd1-425d-94f7-17d3beddc0fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
9ba5b5dc-ddd1-425d-94f7-17d3beddc0fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
9ba5b5dc-ddd1-425d-94f7-17d3beddc0fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
9ba5b5dc-ddd1-425d-94f7-17d3beddc0fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
9ba5b5dc-ddd1-425d-94f7-17d3beddc0fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
9ba5b5dc-ddd1-425d-94f7-17d3beddc0fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
9ba5b5dc-ddd1-425d-94f7-17d3beddc0fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
9ba5b5dc-ddd1-425d-94f7-17d3beddc0fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
9ba5b5dc-ddd1-425d-94f7-17d3beddc0fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
9ba5b5dc-ddd1-425d-94f7-17d3beddc0fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
9ba5b5dc-ddd1-425d-94f7-17d3beddc0fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
d35bd844-886f-41c3-a66c-539da12912d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Torsades de pointes is associated with a prolonged QT interval (>600 msecs) that helps distinguish it from other forms of polymorphous VT. The longer QT interval can be caused by ionic abnormalities that reduce the repolarizing current of Phase 3 of the cardiac action potential. This makes the myocardium susceptible to early after-depolarizations—the trigger for torsades de pointes. These after-depolarizations do not happen uniformly across the myocardium and are more common in endocardial tissue where the repolarization currents are slower. So torsades de pointes arises from the after-depolarizations causing reentry currents in neighboring tissue.,True,Ventricular Tachycardia,,,,
3cb03e3a-c787-4be8-8184-162107cdccee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Both common garden variety VTs and torsades de pointes can progress to ventricular fibrillation.,True,Ventricular Tachycardia,,,,
8cbfcdc0-7f07-4ec0-8eb2-c41793661977,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Table 1.8: VT summary.,True,Ventricular Tachycardia,,,,
c0a765a9-67ff-4302-8a07-2fb240babe4a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Ventricular Fibrillation,False,Ventricular Fibrillation,,,,
d0eb7ea3-253f-4ffc-a239-ed12d0b40e65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Ventricular fibrillation (VF) occurs when the ventricular rate exceeds 400 bpm. The disorganized and uncoordinated contraction of the myocardium causes cardiac output to fall to catastrophic levels. Rates of survival for out-of-hospital VF are low.,True,Ventricular Fibrillation,,,,
8f542bd1-c003-4448-8cef-04de56d2b1cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
8f542bd1-c003-4448-8cef-04de56d2b1cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
8f542bd1-c003-4448-8cef-04de56d2b1cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
8f542bd1-c003-4448-8cef-04de56d2b1cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
8f542bd1-c003-4448-8cef-04de56d2b1cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
8f542bd1-c003-4448-8cef-04de56d2b1cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
8f542bd1-c003-4448-8cef-04de56d2b1cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
8f542bd1-c003-4448-8cef-04de56d2b1cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
8f542bd1-c003-4448-8cef-04de56d2b1cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
8f542bd1-c003-4448-8cef-04de56d2b1cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
8f542bd1-c003-4448-8cef-04de56d2b1cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
8f542bd1-c003-4448-8cef-04de56d2b1cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
8f542bd1-c003-4448-8cef-04de56d2b1cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
8f542bd1-c003-4448-8cef-04de56d2b1cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
8f542bd1-c003-4448-8cef-04de56d2b1cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
8f542bd1-c003-4448-8cef-04de56d2b1cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
8f542bd1-c003-4448-8cef-04de56d2b1cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
44d29f53-80b0-4ed4-b732-4c4d0eee1072,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Table 1.9: VF summary.,True,Ventricular Fibrillation,,,,
d9b896ca-f2b8-4e49-88dc-8459d25c2581,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,First-Degree Atrioventricular Block,False,First-Degree Atrioventricular Block,,,,
a45c0b73-9bfb-4f67-b6ad-4bb7b513a7ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
a45c0b73-9bfb-4f67-b6ad-4bb7b513a7ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
a45c0b73-9bfb-4f67-b6ad-4bb7b513a7ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
a45c0b73-9bfb-4f67-b6ad-4bb7b513a7ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
a45c0b73-9bfb-4f67-b6ad-4bb7b513a7ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
a45c0b73-9bfb-4f67-b6ad-4bb7b513a7ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
a45c0b73-9bfb-4f67-b6ad-4bb7b513a7ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
a45c0b73-9bfb-4f67-b6ad-4bb7b513a7ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
a45c0b73-9bfb-4f67-b6ad-4bb7b513a7ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
a45c0b73-9bfb-4f67-b6ad-4bb7b513a7ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
a45c0b73-9bfb-4f67-b6ad-4bb7b513a7ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
a45c0b73-9bfb-4f67-b6ad-4bb7b513a7ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
a45c0b73-9bfb-4f67-b6ad-4bb7b513a7ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
a45c0b73-9bfb-4f67-b6ad-4bb7b513a7ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
a45c0b73-9bfb-4f67-b6ad-4bb7b513a7ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
a45c0b73-9bfb-4f67-b6ad-4bb7b513a7ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
a45c0b73-9bfb-4f67-b6ad-4bb7b513a7ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
361aacc2-c209-4d5f-b277-dc50f1eadd3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
361aacc2-c209-4d5f-b277-dc50f1eadd3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
361aacc2-c209-4d5f-b277-dc50f1eadd3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
361aacc2-c209-4d5f-b277-dc50f1eadd3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
361aacc2-c209-4d5f-b277-dc50f1eadd3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
361aacc2-c209-4d5f-b277-dc50f1eadd3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
361aacc2-c209-4d5f-b277-dc50f1eadd3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
361aacc2-c209-4d5f-b277-dc50f1eadd3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
361aacc2-c209-4d5f-b277-dc50f1eadd3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
361aacc2-c209-4d5f-b277-dc50f1eadd3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
361aacc2-c209-4d5f-b277-dc50f1eadd3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
361aacc2-c209-4d5f-b277-dc50f1eadd3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
361aacc2-c209-4d5f-b277-dc50f1eadd3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
361aacc2-c209-4d5f-b277-dc50f1eadd3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
361aacc2-c209-4d5f-b277-dc50f1eadd3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
361aacc2-c209-4d5f-b277-dc50f1eadd3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
361aacc2-c209-4d5f-b277-dc50f1eadd3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
c609fe73-6a57-409e-805e-675d47a33f28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Table 1.10: First-degree block summary.,True,First-Degree Atrioventricular Block,,,,
fa64dc7c-ac5c-44bc-b940-fd7a24855767,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Second-Degree Atrioventricular Block,False,Second-Degree Atrioventricular Block,,,,
55cb1a19-c7e7-4b0e-bfa6-b7fa63e345be,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A second-degree atrioventricular block also has changes in P-R interval, but it starts to show failure of the P-wave to propagate a QRS complex every time (i.e., intermittently the depolarization fails to reach the ventricles). The pattern of missed ventricular depolarizations, or blocked P-waves, is often very regular and described as a ratio of P-waves to QRS complex. The way in which the P-R interval changes in relation to the blocked P-waves produces subclassifications of second-degree blocks, Mobitz I and II.",True,Second-Degree Atrioventricular Block,,,,
f325b0a3-af68-4114-84b2-ce2468fda400,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f325b0a3-af68-4114-84b2-ce2468fda400,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f325b0a3-af68-4114-84b2-ce2468fda400,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f325b0a3-af68-4114-84b2-ce2468fda400,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f325b0a3-af68-4114-84b2-ce2468fda400,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f325b0a3-af68-4114-84b2-ce2468fda400,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f325b0a3-af68-4114-84b2-ce2468fda400,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f325b0a3-af68-4114-84b2-ce2468fda400,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f325b0a3-af68-4114-84b2-ce2468fda400,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f325b0a3-af68-4114-84b2-ce2468fda400,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f325b0a3-af68-4114-84b2-ce2468fda400,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f325b0a3-af68-4114-84b2-ce2468fda400,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f325b0a3-af68-4114-84b2-ce2468fda400,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f325b0a3-af68-4114-84b2-ce2468fda400,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f325b0a3-af68-4114-84b2-ce2468fda400,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f325b0a3-af68-4114-84b2-ce2468fda400,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f325b0a3-af68-4114-84b2-ce2468fda400,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
5728ed11-f492-46cb-8869-7028e216da9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
5728ed11-f492-46cb-8869-7028e216da9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
5728ed11-f492-46cb-8869-7028e216da9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
5728ed11-f492-46cb-8869-7028e216da9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
5728ed11-f492-46cb-8869-7028e216da9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
5728ed11-f492-46cb-8869-7028e216da9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
5728ed11-f492-46cb-8869-7028e216da9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
5728ed11-f492-46cb-8869-7028e216da9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
5728ed11-f492-46cb-8869-7028e216da9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
5728ed11-f492-46cb-8869-7028e216da9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
5728ed11-f492-46cb-8869-7028e216da9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
5728ed11-f492-46cb-8869-7028e216da9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
5728ed11-f492-46cb-8869-7028e216da9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
5728ed11-f492-46cb-8869-7028e216da9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
5728ed11-f492-46cb-8869-7028e216da9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
5728ed11-f492-46cb-8869-7028e216da9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
5728ed11-f492-46cb-8869-7028e216da9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
559a91ea-3102-403c-a6dc-e5b998aa1b98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Table 1.11: Second-degree block summary.,True,Second-Degree Atrioventricular Block,,,,
fa5e6509-4780-4785-895c-e0ee03b2a8c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Third-Degree Atrioventricular Block,False,Third-Degree Atrioventricular Block,,,,
57adcc06-65aa-445e-b446-0a7735b77e13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
57adcc06-65aa-445e-b446-0a7735b77e13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
57adcc06-65aa-445e-b446-0a7735b77e13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
57adcc06-65aa-445e-b446-0a7735b77e13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
57adcc06-65aa-445e-b446-0a7735b77e13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
57adcc06-65aa-445e-b446-0a7735b77e13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
57adcc06-65aa-445e-b446-0a7735b77e13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
57adcc06-65aa-445e-b446-0a7735b77e13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
57adcc06-65aa-445e-b446-0a7735b77e13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
57adcc06-65aa-445e-b446-0a7735b77e13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
57adcc06-65aa-445e-b446-0a7735b77e13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
57adcc06-65aa-445e-b446-0a7735b77e13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
57adcc06-65aa-445e-b446-0a7735b77e13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
57adcc06-65aa-445e-b446-0a7735b77e13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
57adcc06-65aa-445e-b446-0a7735b77e13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
57adcc06-65aa-445e-b446-0a7735b77e13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
57adcc06-65aa-445e-b446-0a7735b77e13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
ef513824-c394-4bf1-a583-f79a762e5e5f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Table 1.12: Third-degree block summary.,True,Third-Degree Atrioventricular Block,,,,
2c9ff76a-88a2-48e8-a50a-9b1537d924d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Left Bundle Branch Block,False,Left Bundle Branch Block,,,,
79b4e186-7a0e-4ca2-90c2-8a2557f513ff,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"A left bundle branch block (LBBB) is generated when the conductivity of the His-Purkinje system in the left ventricle is compromised, either through damage or disease. The ECG changes, and criteria for LBBB relate to these changes in conductivity and the left-side location.",True,Left Bundle Branch Block,,,,
a6c7c600-f59e-4d54-8c9a-726004111239,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a6c7c600-f59e-4d54-8c9a-726004111239,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a6c7c600-f59e-4d54-8c9a-726004111239,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a6c7c600-f59e-4d54-8c9a-726004111239,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a6c7c600-f59e-4d54-8c9a-726004111239,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a6c7c600-f59e-4d54-8c9a-726004111239,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a6c7c600-f59e-4d54-8c9a-726004111239,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a6c7c600-f59e-4d54-8c9a-726004111239,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a6c7c600-f59e-4d54-8c9a-726004111239,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a6c7c600-f59e-4d54-8c9a-726004111239,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a6c7c600-f59e-4d54-8c9a-726004111239,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a6c7c600-f59e-4d54-8c9a-726004111239,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a6c7c600-f59e-4d54-8c9a-726004111239,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a6c7c600-f59e-4d54-8c9a-726004111239,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a6c7c600-f59e-4d54-8c9a-726004111239,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a6c7c600-f59e-4d54-8c9a-726004111239,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a6c7c600-f59e-4d54-8c9a-726004111239,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
7380acc0-5bc8-4db3-857a-bd26141ea306,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The lateral leads (I, V5, and V6) normally show a downward deflecting Q-wave as normal septal deflection initially occurs left-to-right (i.e., away from the lateral leads). In LBBB the change in direction to right-to-left, plus the longer duration, eliminates the Q-wave from the lateral leads, and Q-waves will be small in aVL.",True,Left Bundle Branch Block,,,,
cb38c211-16b3-4d82-9a68-6e69b967abfb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
cb38c211-16b3-4d82-9a68-6e69b967abfb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
cb38c211-16b3-4d82-9a68-6e69b967abfb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
cb38c211-16b3-4d82-9a68-6e69b967abfb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
cb38c211-16b3-4d82-9a68-6e69b967abfb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
cb38c211-16b3-4d82-9a68-6e69b967abfb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
cb38c211-16b3-4d82-9a68-6e69b967abfb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
cb38c211-16b3-4d82-9a68-6e69b967abfb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
cb38c211-16b3-4d82-9a68-6e69b967abfb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
cb38c211-16b3-4d82-9a68-6e69b967abfb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
cb38c211-16b3-4d82-9a68-6e69b967abfb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
cb38c211-16b3-4d82-9a68-6e69b967abfb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
cb38c211-16b3-4d82-9a68-6e69b967abfb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
cb38c211-16b3-4d82-9a68-6e69b967abfb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
cb38c211-16b3-4d82-9a68-6e69b967abfb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
cb38c211-16b3-4d82-9a68-6e69b967abfb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
cb38c211-16b3-4d82-9a68-6e69b967abfb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
2b6c1ddb-6433-4508-b59f-ba4eda3fd6c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
2b6c1ddb-6433-4508-b59f-ba4eda3fd6c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
2b6c1ddb-6433-4508-b59f-ba4eda3fd6c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
2b6c1ddb-6433-4508-b59f-ba4eda3fd6c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
2b6c1ddb-6433-4508-b59f-ba4eda3fd6c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
2b6c1ddb-6433-4508-b59f-ba4eda3fd6c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
2b6c1ddb-6433-4508-b59f-ba4eda3fd6c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
2b6c1ddb-6433-4508-b59f-ba4eda3fd6c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
2b6c1ddb-6433-4508-b59f-ba4eda3fd6c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
2b6c1ddb-6433-4508-b59f-ba4eda3fd6c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
2b6c1ddb-6433-4508-b59f-ba4eda3fd6c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
2b6c1ddb-6433-4508-b59f-ba4eda3fd6c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
2b6c1ddb-6433-4508-b59f-ba4eda3fd6c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
2b6c1ddb-6433-4508-b59f-ba4eda3fd6c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
2b6c1ddb-6433-4508-b59f-ba4eda3fd6c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
2b6c1ddb-6433-4508-b59f-ba4eda3fd6c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
2b6c1ddb-6433-4508-b59f-ba4eda3fd6c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
18fdf5fa-68ec-4619-955f-fdedd013433b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Table 1.13: LBBB summary.,True,Left Bundle Branch Block,,,,
72b6a909-f7d3-436c-bedb-f4c4e5e10d5a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Right Bundle Branch Block,False,Right Bundle Branch Block,,,,
8e598727-aadf-4bc3-ab61-c40832a1dba5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The causes and manifestations of a right bundle branch block (RBBB) bear some similarities to those described for LBBB, but of course this time its depolarization of the right ventricle is delayed. Causes of RBBB include ischemic heart disease again as well as other myocardial diseases, but pulmonary issues such as pulmonary embolism and cor pulmonale can be added to the list.",True,Right Bundle Branch Block,,,,
531a98d5-0259-4b5b-9870-6f2aafaa950d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
531a98d5-0259-4b5b-9870-6f2aafaa950d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
531a98d5-0259-4b5b-9870-6f2aafaa950d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
531a98d5-0259-4b5b-9870-6f2aafaa950d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
531a98d5-0259-4b5b-9870-6f2aafaa950d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
531a98d5-0259-4b5b-9870-6f2aafaa950d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
531a98d5-0259-4b5b-9870-6f2aafaa950d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
531a98d5-0259-4b5b-9870-6f2aafaa950d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
531a98d5-0259-4b5b-9870-6f2aafaa950d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
531a98d5-0259-4b5b-9870-6f2aafaa950d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
531a98d5-0259-4b5b-9870-6f2aafaa950d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
531a98d5-0259-4b5b-9870-6f2aafaa950d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
531a98d5-0259-4b5b-9870-6f2aafaa950d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
531a98d5-0259-4b5b-9870-6f2aafaa950d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
531a98d5-0259-4b5b-9870-6f2aafaa950d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
531a98d5-0259-4b5b-9870-6f2aafaa950d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
531a98d5-0259-4b5b-9870-6f2aafaa950d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
4d52077a-4b11-45e7-b978-d7367369802a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Table 1.14: RBBB summary.,True,Right Bundle Branch Block,,,,
c8be9d99-43e2-43f7-8ce2-f6871863843b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Wolff-Parkinson-White Syndrome,False,Wolff-Parkinson-White Syndrome,,,,
47aaa7c0-d4ec-47bc-8020-8047ddf542e5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Normally the only electrical connection between the atria and the ventricles is the AV node. Otherwise the fibrous skeleton of the heart electrically insulates the atria from the ventricles. In Wolff-Parkinson-White (WPW) syndrome, that insulation is incomplete, and an “accessory pathway” connects the electrical system of the atria directly to the ventricles. If you think of the AV node as a bridge over the fibrous wall with regulated access, the accessory pathway is like a pathological tunnel under it with no regulation.",True,Wolff-Parkinson-White Syndrome,,,,
d00c8731-f27e-422d-9268-7e0682e27679,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
d00c8731-f27e-422d-9268-7e0682e27679,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
d00c8731-f27e-422d-9268-7e0682e27679,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
d00c8731-f27e-422d-9268-7e0682e27679,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
d00c8731-f27e-422d-9268-7e0682e27679,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
d00c8731-f27e-422d-9268-7e0682e27679,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
d00c8731-f27e-422d-9268-7e0682e27679,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
d00c8731-f27e-422d-9268-7e0682e27679,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
d00c8731-f27e-422d-9268-7e0682e27679,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
d00c8731-f27e-422d-9268-7e0682e27679,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
d00c8731-f27e-422d-9268-7e0682e27679,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
d00c8731-f27e-422d-9268-7e0682e27679,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
d00c8731-f27e-422d-9268-7e0682e27679,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
d00c8731-f27e-422d-9268-7e0682e27679,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
d00c8731-f27e-422d-9268-7e0682e27679,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
d00c8731-f27e-422d-9268-7e0682e27679,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
d00c8731-f27e-422d-9268-7e0682e27679,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
6859a2d5-64fa-48a0-9d49-0f7fd000894e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"WPW syndrome is often asymptomatic, and patients do not require immediate treatment. However, if atrial fibrillation occurs in a WPW patient, the accessory pathway can allow the atrial fibrillation waves through to the ventricle (with no AV nodal refractory period to prevent them). Consequently a high ventricular rate is seen, and the risk of ventricular fibrillation being established means immediate clinical attention is required.",True,Wolff-Parkinson-White Syndrome,,,,
476d29c1-c5eb-4fa9-bee8-2db1657ed20c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Hyper- and Hypocalcemia,False,Hyper- and Hypocalcemia,,,,
ac1bf148-8cee-42b1-87d3-6b8d4442b525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
ac1bf148-8cee-42b1-87d3-6b8d4442b525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
ac1bf148-8cee-42b1-87d3-6b8d4442b525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
ac1bf148-8cee-42b1-87d3-6b8d4442b525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
ac1bf148-8cee-42b1-87d3-6b8d4442b525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
ac1bf148-8cee-42b1-87d3-6b8d4442b525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
ac1bf148-8cee-42b1-87d3-6b8d4442b525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
ac1bf148-8cee-42b1-87d3-6b8d4442b525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
ac1bf148-8cee-42b1-87d3-6b8d4442b525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
ac1bf148-8cee-42b1-87d3-6b8d4442b525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
ac1bf148-8cee-42b1-87d3-6b8d4442b525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
ac1bf148-8cee-42b1-87d3-6b8d4442b525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
ac1bf148-8cee-42b1-87d3-6b8d4442b525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
ac1bf148-8cee-42b1-87d3-6b8d4442b525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
ac1bf148-8cee-42b1-87d3-6b8d4442b525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
ac1bf148-8cee-42b1-87d3-6b8d4442b525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
ac1bf148-8cee-42b1-87d3-6b8d4442b525,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
18e0e901-7619-40fd-9c98-5ef9a55c186d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
18e0e901-7619-40fd-9c98-5ef9a55c186d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
18e0e901-7619-40fd-9c98-5ef9a55c186d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
18e0e901-7619-40fd-9c98-5ef9a55c186d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
18e0e901-7619-40fd-9c98-5ef9a55c186d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
18e0e901-7619-40fd-9c98-5ef9a55c186d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
18e0e901-7619-40fd-9c98-5ef9a55c186d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
18e0e901-7619-40fd-9c98-5ef9a55c186d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
18e0e901-7619-40fd-9c98-5ef9a55c186d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
18e0e901-7619-40fd-9c98-5ef9a55c186d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
18e0e901-7619-40fd-9c98-5ef9a55c186d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
18e0e901-7619-40fd-9c98-5ef9a55c186d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
18e0e901-7619-40fd-9c98-5ef9a55c186d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
18e0e901-7619-40fd-9c98-5ef9a55c186d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
18e0e901-7619-40fd-9c98-5ef9a55c186d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
18e0e901-7619-40fd-9c98-5ef9a55c186d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
18e0e901-7619-40fd-9c98-5ef9a55c186d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
7bdde3a5-f472-4507-9c88-16d86f8c7215,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Table 1.16: Hyper- and hypocalcemia summary.,True,Hyper- and Hypocalcemia,,,,
6f367c36-4d6a-4784-8957-7734bd5b7553,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Hyper- and Hypokalemia,False,Hyper- and Hypokalemia,,,,
c76126b2-ff0c-41a4-92dc-e8156135cd70,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"The pathophysiology is not as simple as changes in extracellular K+ changing the electrochemical gradient for K+. Because of potassium’s role in maintaining the resting membrane potential, shifts in extracellular potassium can also influence the activity of Na+ and Ca++ channels.",True,Hyper- and Hypokalemia,,,,
cd178941-e369-4345-93e1-6e8c5dc7f3fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
cd178941-e369-4345-93e1-6e8c5dc7f3fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
cd178941-e369-4345-93e1-6e8c5dc7f3fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
cd178941-e369-4345-93e1-6e8c5dc7f3fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
cd178941-e369-4345-93e1-6e8c5dc7f3fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
cd178941-e369-4345-93e1-6e8c5dc7f3fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
cd178941-e369-4345-93e1-6e8c5dc7f3fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
cd178941-e369-4345-93e1-6e8c5dc7f3fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
cd178941-e369-4345-93e1-6e8c5dc7f3fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
cd178941-e369-4345-93e1-6e8c5dc7f3fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
cd178941-e369-4345-93e1-6e8c5dc7f3fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
cd178941-e369-4345-93e1-6e8c5dc7f3fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
cd178941-e369-4345-93e1-6e8c5dc7f3fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
cd178941-e369-4345-93e1-6e8c5dc7f3fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
cd178941-e369-4345-93e1-6e8c5dc7f3fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
cd178941-e369-4345-93e1-6e8c5dc7f3fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
cd178941-e369-4345-93e1-6e8c5dc7f3fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
71dedca6-4cb8-4bd6-8fd9-d3819f4fac43,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"As hypokalemia also inhibits Na+-K+ ATPase, Na+ accumulates inside the cell. This in turn leads to an accumulation of Ca++ because of a subsequent failure of the Na+-Ca++ exchanger. Extended presence of these two positive ions inside the myocyte prolongs the action potential and may manifest as an increased width and amplitude of the P-wave.",True,Hyper- and Hypokalemia,,,,
74784ccd-238d-4773-a695-ac501af65c82,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"As hypokalemia worsens, the problems with K+ conductance and repolarization increase, and the myocardium becomes susceptible to early after-depolarization (EAD) arrhythmias.",True,Hyper- and Hypokalemia,,,,
fed29eab-4c49-4a09-9fa2-a546a33f974f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fed29eab-4c49-4a09-9fa2-a546a33f974f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fed29eab-4c49-4a09-9fa2-a546a33f974f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fed29eab-4c49-4a09-9fa2-a546a33f974f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fed29eab-4c49-4a09-9fa2-a546a33f974f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fed29eab-4c49-4a09-9fa2-a546a33f974f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fed29eab-4c49-4a09-9fa2-a546a33f974f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fed29eab-4c49-4a09-9fa2-a546a33f974f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fed29eab-4c49-4a09-9fa2-a546a33f974f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fed29eab-4c49-4a09-9fa2-a546a33f974f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fed29eab-4c49-4a09-9fa2-a546a33f974f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fed29eab-4c49-4a09-9fa2-a546a33f974f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fed29eab-4c49-4a09-9fa2-a546a33f974f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fed29eab-4c49-4a09-9fa2-a546a33f974f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fed29eab-4c49-4a09-9fa2-a546a33f974f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fed29eab-4c49-4a09-9fa2-a546a33f974f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fed29eab-4c49-4a09-9fa2-a546a33f974f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
7e44e722-6fe6-4707-b7ca-93e05ccbe45d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7e44e722-6fe6-4707-b7ca-93e05ccbe45d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7e44e722-6fe6-4707-b7ca-93e05ccbe45d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7e44e722-6fe6-4707-b7ca-93e05ccbe45d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7e44e722-6fe6-4707-b7ca-93e05ccbe45d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7e44e722-6fe6-4707-b7ca-93e05ccbe45d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7e44e722-6fe6-4707-b7ca-93e05ccbe45d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7e44e722-6fe6-4707-b7ca-93e05ccbe45d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7e44e722-6fe6-4707-b7ca-93e05ccbe45d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7e44e722-6fe6-4707-b7ca-93e05ccbe45d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7e44e722-6fe6-4707-b7ca-93e05ccbe45d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7e44e722-6fe6-4707-b7ca-93e05ccbe45d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7e44e722-6fe6-4707-b7ca-93e05ccbe45d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7e44e722-6fe6-4707-b7ca-93e05ccbe45d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7e44e722-6fe6-4707-b7ca-93e05ccbe45d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7e44e722-6fe6-4707-b7ca-93e05ccbe45d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7e44e722-6fe6-4707-b7ca-93e05ccbe45d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
ef056c24-248a-4008-b6ed-4258ce47b3df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
ef056c24-248a-4008-b6ed-4258ce47b3df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
ef056c24-248a-4008-b6ed-4258ce47b3df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
ef056c24-248a-4008-b6ed-4258ce47b3df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
ef056c24-248a-4008-b6ed-4258ce47b3df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
ef056c24-248a-4008-b6ed-4258ce47b3df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
ef056c24-248a-4008-b6ed-4258ce47b3df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
ef056c24-248a-4008-b6ed-4258ce47b3df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
ef056c24-248a-4008-b6ed-4258ce47b3df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
ef056c24-248a-4008-b6ed-4258ce47b3df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
ef056c24-248a-4008-b6ed-4258ce47b3df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
ef056c24-248a-4008-b6ed-4258ce47b3df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
ef056c24-248a-4008-b6ed-4258ce47b3df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
ef056c24-248a-4008-b6ed-4258ce47b3df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
ef056c24-248a-4008-b6ed-4258ce47b3df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
ef056c24-248a-4008-b6ed-4258ce47b3df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
ef056c24-248a-4008-b6ed-4258ce47b3df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
4d8321df-3db5-456c-b8d0-f1298226de28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
4d8321df-3db5-456c-b8d0-f1298226de28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
4d8321df-3db5-456c-b8d0-f1298226de28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
4d8321df-3db5-456c-b8d0-f1298226de28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
4d8321df-3db5-456c-b8d0-f1298226de28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
4d8321df-3db5-456c-b8d0-f1298226de28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
4d8321df-3db5-456c-b8d0-f1298226de28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
4d8321df-3db5-456c-b8d0-f1298226de28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
4d8321df-3db5-456c-b8d0-f1298226de28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
4d8321df-3db5-456c-b8d0-f1298226de28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
4d8321df-3db5-456c-b8d0-f1298226de28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
4d8321df-3db5-456c-b8d0-f1298226de28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
4d8321df-3db5-456c-b8d0-f1298226de28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
4d8321df-3db5-456c-b8d0-f1298226de28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
4d8321df-3db5-456c-b8d0-f1298226de28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
4d8321df-3db5-456c-b8d0-f1298226de28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
4d8321df-3db5-456c-b8d0-f1298226de28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
842fcb4a-6768-4fa7-a8b6-5950a78b000e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Table 1.17: Hypo- and hyperkalemia summary.,True,Hyper- and Hypokalemia,,,,
cef76ba0-9d9a-4618-9c90-224179f02d4f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"References, resources, and further reading",False,"References, resources, and further reading",,,,
2709e2ae-f386-4f7d-87e9-8e3e2a12e208,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,Text,False,Text,,,,
6e5207f7-068b-40ad-b79c-74d309e18fc5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Burns, Ed, and Robert Buttner. Hypercalcaemia. Lift in the Fast Lane, 2021. https://litfl.com/hypercalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
bb5dcfa6-0b37-4100-ad13-179e4a70ded9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Burns, Ed, and Robert Buttner. Hypocalcaemia. Life in the Fast Lane, 2021. https://litfl.com/hypocalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
2cad4746-b582-4e42-a68f-58911b956d53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Buttner, Robert, and Ed Burns. Hyperkalaemia. Life in the Fast Lane. https://litfl.com/hyperkalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
7c33d994-a345-4595-934f-58e6319e52e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Buttner, Robert, and Ed Burns. Hypokalaemia. Life in the Fast Lane, 2021. https://litfl.com/hypokalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
75bc8bc8-d2f3-4652-9713-e4854599a74b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Chhabra, Lovely, Amandeep Goyal, and Michael D. Benham. Wolff Parkinson White Syndrome. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK554437/, CC BY 4.0.",True,Text,,,,
85a5c5bf-18e5-44c4-beaf-5c8f030de9f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Custer, Adam M., Varun S. Yelamanchili, and Sarah L. Lappin. Multifocal Atrial Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459152/, CC BY 4.0.",True,Text,,,,
6c97b106-603c-4bdc-a577-dc1b60b23874,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Farzam, Khashayar, and John R. Richards. Premature Ventricular Contraction. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532991/, CC BY 4.0.",True,Text,,,,
9d6f716c-e917-49f9-9e8d-cd04f1e7192d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Foth, Christopher, Manesh Kumar Gangwani, and Heidi Alvey. Ventricular Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532954/, CC BY 4.0.",True,Text,,,,
bac8000d-a47d-4692-b6d7-830178e7515e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Hafeez, Yamama, and Shamai A. Grossman. Sinus Bradycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK493201/, CC BY 4.0.",True,Text,,,,
eee8fd1c-bae7-41a9-acd3-99d1e0090ef5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Harkness, Weston T., and Mary Hicks. Right Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK507872/, CC BY 4.0.",True,Text,,,,
90516585-455d-4d0c-bc3b-51b3bcbc31b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Heaton, Joseph, and Srikanth Yandrapalli. Premature Atrial Contractions. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK559204/, CC BY 4.0.",True,Text,,,,
a7f73fad-a2db-4f31-9438-2e6cbab7f1fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Kashou, Anthony H., Amandeep Goyal, Tran Nguyen, and Lovely Chhabra. Atrioventricular Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459147/, CC BY 4.0.",True,Text,,,,
913e7318-3212-4b65-bfc7-303c4bcc131a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,“Learn the Heart.” Healio. https://www.healio.com/cardiology/learn-the-heart.,True,Text,,,,
f54ed3b9-50e3-4f85-b69c-b6fe4041e5b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Ludhwani, Dipesh, Amandeep Goyal, and Mandar Jagtap. Ventricular Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK537120/, CC BY 4.0.",True,Text,,,,
7ed3e0aa-84d7-466e-ade8-2548cd7b2e1a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Nesheiwat, Zeid, Amandeep Goyal, and Mandar Jagtap. Atrial Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK526072/, CC BY 4.0.",True,Text,,,,
126d605a-d9a4-43d7-a122-e81dbc0d4271,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Pipilas, Daniel C., Bruce A. Koplan, and Leonard S. Lilly. “The Electrocardiogram.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 4. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
00f6a2ad-68ed-4fe7-a757-8c6a198d4598,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Rodriguez Ziccardi, Mary, Amandeep Goyal, and Christopher V. Maani. Atrial Flutter. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK540985/, CC BY 4.0.",True,Text,,,,
0b0be905-bd92-4438-ab5e-43c2c490adae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-11,"Scherbak, Dmitriy, and Gregory J. Hicks. Left Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK482167/, CC BY 4.0.",True,Text,,,,
215913a5-6be5-4dc0-98ad-1f5d76f9d949,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,USMLE,False,USMLE,,,,
8718b864-d775-4da1-aa8a-2a2dbedd170a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
8718b864-d775-4da1-aa8a-2a2dbedd170a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
8718b864-d775-4da1-aa8a-2a2dbedd170a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
8718b864-d775-4da1-aa8a-2a2dbedd170a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
8718b864-d775-4da1-aa8a-2a2dbedd170a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
8718b864-d775-4da1-aa8a-2a2dbedd170a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
8718b864-d775-4da1-aa8a-2a2dbedd170a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
8718b864-d775-4da1-aa8a-2a2dbedd170a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
8718b864-d775-4da1-aa8a-2a2dbedd170a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
8718b864-d775-4da1-aa8a-2a2dbedd170a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
8718b864-d775-4da1-aa8a-2a2dbedd170a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
8718b864-d775-4da1-aa8a-2a2dbedd170a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
8718b864-d775-4da1-aa8a-2a2dbedd170a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
8718b864-d775-4da1-aa8a-2a2dbedd170a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
8718b864-d775-4da1-aa8a-2a2dbedd170a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
8718b864-d775-4da1-aa8a-2a2dbedd170a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
8718b864-d775-4da1-aa8a-2a2dbedd170a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
05f17916-ef14-4835-b9b7-0441e5450306,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,10q22,False,10q22,,,,
9d9c812a-ecca-45ba-9b22-0ba7f9199c18,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,q24,False,q24,,,,
480e49a3-85cd-417c-8d51-b0462e64cfd3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,fibrillatory,False,fibrillatory,,,,
8e6d1135-44e1-4891-adfe-589c52a10728,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8e6d1135-44e1-4891-adfe-589c52a10728,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8e6d1135-44e1-4891-adfe-589c52a10728,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8e6d1135-44e1-4891-adfe-589c52a10728,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8e6d1135-44e1-4891-adfe-589c52a10728,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8e6d1135-44e1-4891-adfe-589c52a10728,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8e6d1135-44e1-4891-adfe-589c52a10728,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8e6d1135-44e1-4891-adfe-589c52a10728,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8e6d1135-44e1-4891-adfe-589c52a10728,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8e6d1135-44e1-4891-adfe-589c52a10728,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8e6d1135-44e1-4891-adfe-589c52a10728,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8e6d1135-44e1-4891-adfe-589c52a10728,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8e6d1135-44e1-4891-adfe-589c52a10728,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8e6d1135-44e1-4891-adfe-589c52a10728,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8e6d1135-44e1-4891-adfe-589c52a10728,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8e6d1135-44e1-4891-adfe-589c52a10728,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8e6d1135-44e1-4891-adfe-589c52a10728,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
00679e9d-e06c-4838-9c02-e884b6826b91,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Table 1.1: Atrial fibrillation summary.,True,fibrillatory,,,,
a42caed2-32fc-4638-902b-2e88e6473dd6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Atrial Flutter,False,Atrial Flutter,,,,
fd42c4ee-c19e-4b91-898f-5e63b571c987,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
fd42c4ee-c19e-4b91-898f-5e63b571c987,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
fd42c4ee-c19e-4b91-898f-5e63b571c987,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
fd42c4ee-c19e-4b91-898f-5e63b571c987,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
fd42c4ee-c19e-4b91-898f-5e63b571c987,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
fd42c4ee-c19e-4b91-898f-5e63b571c987,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
fd42c4ee-c19e-4b91-898f-5e63b571c987,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
fd42c4ee-c19e-4b91-898f-5e63b571c987,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
fd42c4ee-c19e-4b91-898f-5e63b571c987,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
fd42c4ee-c19e-4b91-898f-5e63b571c987,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
fd42c4ee-c19e-4b91-898f-5e63b571c987,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
fd42c4ee-c19e-4b91-898f-5e63b571c987,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
fd42c4ee-c19e-4b91-898f-5e63b571c987,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
fd42c4ee-c19e-4b91-898f-5e63b571c987,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
fd42c4ee-c19e-4b91-898f-5e63b571c987,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
fd42c4ee-c19e-4b91-898f-5e63b571c987,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
fd42c4ee-c19e-4b91-898f-5e63b571c987,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
07ec59b6-93a6-4d8d-9f6e-e31f4754ce90,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,macroreentrant,False,macroreentrant,,,,
b19066f9-cbe4-4fa6-bc93-c0febf43e85a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,cavotricuspid,False,cavotricuspid,,,,
62180554-53f1-4c7e-9f3f-78109540ba36,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"As with atrial fibrillation, the AV node’s refractory period prevents most of the P-waves from progressing to the ventricle, but commonly the AV conduction will be 2-to-1, so with an atrial rate of 300 bpm the ventricular rate will be 150 bpm. Parasympathetic stimulation or changes in AV node refractoriness can modify how many P-waves pass into the ventricle, but the the resultant rhythm is “regularly irregular.” When the heart rate is elevated, then distinguishing flutter from fibrillation becomes challenging and slowing ventricular rate pharmaceutically (adenosine) helps the flutter waves reemerge for a definitive diagnosis to be made.",True,cavotricuspid,,,,
59f67444-63b8-4280-8c07-e90feef6d612,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Table 1.2: Atrial flutter summary.,True,cavotricuspid,,,,
0ae2f9d1-a738-484c-aeb5-317df5eecf8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Multifocal Atrial Tachycardia,False,Multifocal Atrial Tachycardia,,,,
840ccd6a-804a-46d9-8108-e0797ef3c4e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
840ccd6a-804a-46d9-8108-e0797ef3c4e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
840ccd6a-804a-46d9-8108-e0797ef3c4e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
840ccd6a-804a-46d9-8108-e0797ef3c4e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
840ccd6a-804a-46d9-8108-e0797ef3c4e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
840ccd6a-804a-46d9-8108-e0797ef3c4e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
840ccd6a-804a-46d9-8108-e0797ef3c4e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
840ccd6a-804a-46d9-8108-e0797ef3c4e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
840ccd6a-804a-46d9-8108-e0797ef3c4e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
840ccd6a-804a-46d9-8108-e0797ef3c4e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
840ccd6a-804a-46d9-8108-e0797ef3c4e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
840ccd6a-804a-46d9-8108-e0797ef3c4e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
840ccd6a-804a-46d9-8108-e0797ef3c4e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
840ccd6a-804a-46d9-8108-e0797ef3c4e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
840ccd6a-804a-46d9-8108-e0797ef3c4e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
840ccd6a-804a-46d9-8108-e0797ef3c4e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
840ccd6a-804a-46d9-8108-e0797ef3c4e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
97e134d9-c224-48d0-86b2-2843e2a9c032,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"MAT frequently occurs in the setting of severe lung disease and, more specifically, during an exacerbation of lung disease. This rhythm is benign, and once the underlying lung disease is treated, it should resolve.",True,Multifocal Atrial Tachycardia,,,,
7b833773-5e08-40d0-be8f-ca059eb62437,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Table 1.3: MAT summary.,True,Multifocal Atrial Tachycardia,,,,
008a453a-3b23-4dd6-9dc2-79f628b534d8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Premature Atrial Contraction,False,Premature Atrial Contraction,,,,
ad2f3049-dd56-4037-b24a-bbf51aa6168d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A premature atrial contraction (PAC) is generated by a depolarization instigated outside of the SA node. This produces an extra P-wave, and consequently a shortening from previous P-P intervals is seen. The aberrant P-wave also has a different morphology from a sinus P-wave because of its different anatomical origin.",True,Premature Atrial Contraction,,,,
95cb830e-f50d-4565-957f-6a9e1c704a3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
95cb830e-f50d-4565-957f-6a9e1c704a3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
95cb830e-f50d-4565-957f-6a9e1c704a3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
95cb830e-f50d-4565-957f-6a9e1c704a3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
95cb830e-f50d-4565-957f-6a9e1c704a3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
95cb830e-f50d-4565-957f-6a9e1c704a3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
95cb830e-f50d-4565-957f-6a9e1c704a3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
95cb830e-f50d-4565-957f-6a9e1c704a3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
95cb830e-f50d-4565-957f-6a9e1c704a3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
95cb830e-f50d-4565-957f-6a9e1c704a3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
95cb830e-f50d-4565-957f-6a9e1c704a3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
95cb830e-f50d-4565-957f-6a9e1c704a3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
95cb830e-f50d-4565-957f-6a9e1c704a3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
95cb830e-f50d-4565-957f-6a9e1c704a3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
95cb830e-f50d-4565-957f-6a9e1c704a3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
95cb830e-f50d-4565-957f-6a9e1c704a3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
95cb830e-f50d-4565-957f-6a9e1c704a3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
5c9410d4-1e34-4635-8331-2b12e68a0c9b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"If a PAC occurs when the AV node has not yet recovered from its refractory period, the PAC will fail to conduct to the ventricles; meaning the PAC will not be followed by a QRS complex or the ectopic P-R interval will be prolonged. The ECG will show a premature, ectopic P-wave and then no QRS complex afterward. When this occurs along with bigeminy, the ECG can appear as if there is sinus bradycardia.",True,Premature Atrial Contraction,,,,
bc0eac8e-f0bc-4919-932f-5132daa20d74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Table 1.4: PAC summary.,True,Premature Atrial Contraction,,,,
4aa98264-f8d8-4fcb-b293-b9cf3c357f3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Sinus Bradycardia,False,Sinus Bradycardia,,,,
6d442f6b-a611-46cb-87ec-151d7e086d1a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Sinus bradycardia denotes a sinus rhythm below 60 bpm. Otherwise the ECG waveform is normal on an ECG with an upright P-wave in lead II preceding every QRS complex. There are many intrinsic causes associated with the heart itself, as well as extrinsic causes, some of which are listed table 1.5. Sinus bradycardia is usually asymptomatic as rates of 40–50 bpm can maintain hemodynamic stability. Rates below this can produce symptoms of fatigue, dizziness, and dyspnea on exertion.",True,Sinus Bradycardia,,,,
b6efdde0-abcb-42a5-9491-21241848e50e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Table 1.5: Intrinsic and extrinsic causes associated with the heart.,True,Sinus Bradycardia,,,,
3efd21d6-664e-4eda-904c-514dc0c4a7f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Table 1.6: Sinus bradycardia summary.,True,Sinus Bradycardia,,,,
681dbb8b-2ed2-43d1-b67c-09e996058547,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Premature Ventricular Contractions,False,Premature Ventricular Contractions,,,,
072e44c0-f582-452b-ba87-a02ba643c4a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
072e44c0-f582-452b-ba87-a02ba643c4a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
072e44c0-f582-452b-ba87-a02ba643c4a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
072e44c0-f582-452b-ba87-a02ba643c4a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
072e44c0-f582-452b-ba87-a02ba643c4a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
072e44c0-f582-452b-ba87-a02ba643c4a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
072e44c0-f582-452b-ba87-a02ba643c4a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
072e44c0-f582-452b-ba87-a02ba643c4a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
072e44c0-f582-452b-ba87-a02ba643c4a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
072e44c0-f582-452b-ba87-a02ba643c4a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
072e44c0-f582-452b-ba87-a02ba643c4a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
072e44c0-f582-452b-ba87-a02ba643c4a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
072e44c0-f582-452b-ba87-a02ba643c4a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
072e44c0-f582-452b-ba87-a02ba643c4a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
072e44c0-f582-452b-ba87-a02ba643c4a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
072e44c0-f582-452b-ba87-a02ba643c4a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
072e44c0-f582-452b-ba87-a02ba643c4a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
0a567a9d-1ba3-4271-86d4-4a547c9b53a1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Table 1.7: PVC summary.,True,Premature Ventricular Contractions,,,,
656832a5-0269-406a-9971-215e31100e6f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Ventricular Tachycardia,False,Ventricular Tachycardia,,,,
c31f2fbe-1128-46b8-afba-dbad7d55f012,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Ventricular tachycardia (VT) is caused by reentry currents being established in the ventricular myocardium or groups of ventricular myocytes that have aberrant electrical behavior. As such, VT is usually caused by underlying cardiac disease.",True,Ventricular Tachycardia,,,,
a5f91f23-1c61-44da-ab4a-bd2a32957cf2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Like a PVC, the aberrant depolarizations do not follow the normal conduction pathways so are wide (>120 msecs), but unlike a PVC, VT involves a ventricular rate >100 bpm. With disorganized contractility and reduced filling time, VT can lead to hemodynamic instability and severe hypotension—hence it is life threatening.",True,Ventricular Tachycardia,,,,
dcb3ebfd-10ac-489d-a1bb-d53d0512221b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The QRS morphology in VT is highly variable between patients and depends on where the arrhythmia originates. Consequently there are several ways to classify VT based on duration, symptoms, QRS morphology, rate, and origin.",True,Ventricular Tachycardia,,,,
a5c1a72c-9cbb-4e7b-8fd4-61873d88ea09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Sustained VT is any VT that lasts for more than 30 seconds or is symptomatic. Nonsustained VT lasts for less than 30 seconds and is asymptomatic.,True,Ventricular Tachycardia,,,,
b1198a99-5492-4356-8529-193a446de527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b1198a99-5492-4356-8529-193a446de527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b1198a99-5492-4356-8529-193a446de527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b1198a99-5492-4356-8529-193a446de527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b1198a99-5492-4356-8529-193a446de527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b1198a99-5492-4356-8529-193a446de527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b1198a99-5492-4356-8529-193a446de527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b1198a99-5492-4356-8529-193a446de527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b1198a99-5492-4356-8529-193a446de527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b1198a99-5492-4356-8529-193a446de527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b1198a99-5492-4356-8529-193a446de527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b1198a99-5492-4356-8529-193a446de527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b1198a99-5492-4356-8529-193a446de527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b1198a99-5492-4356-8529-193a446de527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b1198a99-5492-4356-8529-193a446de527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b1198a99-5492-4356-8529-193a446de527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b1198a99-5492-4356-8529-193a446de527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
21b4c503-78c5-4b89-8ebf-4e3cc440e2dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
21b4c503-78c5-4b89-8ebf-4e3cc440e2dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
21b4c503-78c5-4b89-8ebf-4e3cc440e2dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
21b4c503-78c5-4b89-8ebf-4e3cc440e2dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
21b4c503-78c5-4b89-8ebf-4e3cc440e2dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
21b4c503-78c5-4b89-8ebf-4e3cc440e2dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
21b4c503-78c5-4b89-8ebf-4e3cc440e2dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
21b4c503-78c5-4b89-8ebf-4e3cc440e2dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
21b4c503-78c5-4b89-8ebf-4e3cc440e2dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
21b4c503-78c5-4b89-8ebf-4e3cc440e2dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
21b4c503-78c5-4b89-8ebf-4e3cc440e2dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
21b4c503-78c5-4b89-8ebf-4e3cc440e2dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
21b4c503-78c5-4b89-8ebf-4e3cc440e2dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
21b4c503-78c5-4b89-8ebf-4e3cc440e2dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
21b4c503-78c5-4b89-8ebf-4e3cc440e2dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
21b4c503-78c5-4b89-8ebf-4e3cc440e2dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
21b4c503-78c5-4b89-8ebf-4e3cc440e2dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
e70c0fc0-d39b-4e90-b950-4274cb340475,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Torsades de pointes is associated with a prolonged QT interval (>600 msecs) that helps distinguish it from other forms of polymorphous VT. The longer QT interval can be caused by ionic abnormalities that reduce the repolarizing current of Phase 3 of the cardiac action potential. This makes the myocardium susceptible to early after-depolarizations—the trigger for torsades de pointes. These after-depolarizations do not happen uniformly across the myocardium and are more common in endocardial tissue where the repolarization currents are slower. So torsades de pointes arises from the after-depolarizations causing reentry currents in neighboring tissue.,True,Ventricular Tachycardia,,,,
69913ef8-39e9-4331-97bc-b4f9c944b6d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Both common garden variety VTs and torsades de pointes can progress to ventricular fibrillation.,True,Ventricular Tachycardia,,,,
1a18e92a-2e53-4462-bbc1-b5ba7fc36a36,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Table 1.8: VT summary.,True,Ventricular Tachycardia,,,,
02796ba1-d054-4198-9e21-1a1f5e074d40,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Ventricular Fibrillation,False,Ventricular Fibrillation,,,,
0f4fdf3b-3396-4556-b3b6-457f468ec71c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Ventricular fibrillation (VF) occurs when the ventricular rate exceeds 400 bpm. The disorganized and uncoordinated contraction of the myocardium causes cardiac output to fall to catastrophic levels. Rates of survival for out-of-hospital VF are low.,True,Ventricular Fibrillation,,,,
968f9ee4-73df-40db-bab1-5fd5dd7f079a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
968f9ee4-73df-40db-bab1-5fd5dd7f079a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
968f9ee4-73df-40db-bab1-5fd5dd7f079a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
968f9ee4-73df-40db-bab1-5fd5dd7f079a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
968f9ee4-73df-40db-bab1-5fd5dd7f079a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
968f9ee4-73df-40db-bab1-5fd5dd7f079a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
968f9ee4-73df-40db-bab1-5fd5dd7f079a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
968f9ee4-73df-40db-bab1-5fd5dd7f079a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
968f9ee4-73df-40db-bab1-5fd5dd7f079a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
968f9ee4-73df-40db-bab1-5fd5dd7f079a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
968f9ee4-73df-40db-bab1-5fd5dd7f079a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
968f9ee4-73df-40db-bab1-5fd5dd7f079a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
968f9ee4-73df-40db-bab1-5fd5dd7f079a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
968f9ee4-73df-40db-bab1-5fd5dd7f079a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
968f9ee4-73df-40db-bab1-5fd5dd7f079a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
968f9ee4-73df-40db-bab1-5fd5dd7f079a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
968f9ee4-73df-40db-bab1-5fd5dd7f079a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
5599ae1a-1440-4fb1-81d6-abc8bce394fd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Table 1.9: VF summary.,True,Ventricular Fibrillation,,,,
1936e753-f696-43f2-b4c4-b6f63c07bc0f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,First-Degree Atrioventricular Block,False,First-Degree Atrioventricular Block,,,,
ba601e42-7bba-4098-ad27-87071b095fd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba601e42-7bba-4098-ad27-87071b095fd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba601e42-7bba-4098-ad27-87071b095fd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba601e42-7bba-4098-ad27-87071b095fd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba601e42-7bba-4098-ad27-87071b095fd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba601e42-7bba-4098-ad27-87071b095fd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba601e42-7bba-4098-ad27-87071b095fd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba601e42-7bba-4098-ad27-87071b095fd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba601e42-7bba-4098-ad27-87071b095fd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba601e42-7bba-4098-ad27-87071b095fd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba601e42-7bba-4098-ad27-87071b095fd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba601e42-7bba-4098-ad27-87071b095fd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba601e42-7bba-4098-ad27-87071b095fd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba601e42-7bba-4098-ad27-87071b095fd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba601e42-7bba-4098-ad27-87071b095fd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba601e42-7bba-4098-ad27-87071b095fd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba601e42-7bba-4098-ad27-87071b095fd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d97aba07-f928-4b62-93f7-55340051b054,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d97aba07-f928-4b62-93f7-55340051b054,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d97aba07-f928-4b62-93f7-55340051b054,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d97aba07-f928-4b62-93f7-55340051b054,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d97aba07-f928-4b62-93f7-55340051b054,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d97aba07-f928-4b62-93f7-55340051b054,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d97aba07-f928-4b62-93f7-55340051b054,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d97aba07-f928-4b62-93f7-55340051b054,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d97aba07-f928-4b62-93f7-55340051b054,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d97aba07-f928-4b62-93f7-55340051b054,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d97aba07-f928-4b62-93f7-55340051b054,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d97aba07-f928-4b62-93f7-55340051b054,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d97aba07-f928-4b62-93f7-55340051b054,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d97aba07-f928-4b62-93f7-55340051b054,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d97aba07-f928-4b62-93f7-55340051b054,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d97aba07-f928-4b62-93f7-55340051b054,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d97aba07-f928-4b62-93f7-55340051b054,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
2b0e6b09-99df-4c4b-9bb8-46c011df8ec0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Table 1.10: First-degree block summary.,True,First-Degree Atrioventricular Block,,,,
6407bc40-e99c-4421-9e7f-7d1254c8d1c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Second-Degree Atrioventricular Block,False,Second-Degree Atrioventricular Block,,,,
3e6b339a-e084-4e24-9bff-c57997d93875,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A second-degree atrioventricular block also has changes in P-R interval, but it starts to show failure of the P-wave to propagate a QRS complex every time (i.e., intermittently the depolarization fails to reach the ventricles). The pattern of missed ventricular depolarizations, or blocked P-waves, is often very regular and described as a ratio of P-waves to QRS complex. The way in which the P-R interval changes in relation to the blocked P-waves produces subclassifications of second-degree blocks, Mobitz I and II.",True,Second-Degree Atrioventricular Block,,,,
f9b0e8bb-9b13-45d7-a1b8-7df69d097d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9b0e8bb-9b13-45d7-a1b8-7df69d097d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9b0e8bb-9b13-45d7-a1b8-7df69d097d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9b0e8bb-9b13-45d7-a1b8-7df69d097d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9b0e8bb-9b13-45d7-a1b8-7df69d097d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9b0e8bb-9b13-45d7-a1b8-7df69d097d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9b0e8bb-9b13-45d7-a1b8-7df69d097d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9b0e8bb-9b13-45d7-a1b8-7df69d097d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9b0e8bb-9b13-45d7-a1b8-7df69d097d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9b0e8bb-9b13-45d7-a1b8-7df69d097d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9b0e8bb-9b13-45d7-a1b8-7df69d097d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9b0e8bb-9b13-45d7-a1b8-7df69d097d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9b0e8bb-9b13-45d7-a1b8-7df69d097d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9b0e8bb-9b13-45d7-a1b8-7df69d097d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9b0e8bb-9b13-45d7-a1b8-7df69d097d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9b0e8bb-9b13-45d7-a1b8-7df69d097d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
f9b0e8bb-9b13-45d7-a1b8-7df69d097d9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
71fc9edf-95c5-4e89-820f-eff782911341,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
71fc9edf-95c5-4e89-820f-eff782911341,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
71fc9edf-95c5-4e89-820f-eff782911341,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
71fc9edf-95c5-4e89-820f-eff782911341,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
71fc9edf-95c5-4e89-820f-eff782911341,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
71fc9edf-95c5-4e89-820f-eff782911341,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
71fc9edf-95c5-4e89-820f-eff782911341,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
71fc9edf-95c5-4e89-820f-eff782911341,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
71fc9edf-95c5-4e89-820f-eff782911341,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
71fc9edf-95c5-4e89-820f-eff782911341,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
71fc9edf-95c5-4e89-820f-eff782911341,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
71fc9edf-95c5-4e89-820f-eff782911341,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
71fc9edf-95c5-4e89-820f-eff782911341,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
71fc9edf-95c5-4e89-820f-eff782911341,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
71fc9edf-95c5-4e89-820f-eff782911341,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
71fc9edf-95c5-4e89-820f-eff782911341,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
71fc9edf-95c5-4e89-820f-eff782911341,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
7c4ed417-5e2e-4080-899d-4409794ddcc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Table 1.11: Second-degree block summary.,True,Second-Degree Atrioventricular Block,,,,
b5ec2b0b-5776-43a2-bf6b-cd7f09a8e64d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Third-Degree Atrioventricular Block,False,Third-Degree Atrioventricular Block,,,,
95eb1a9e-9077-4387-bac7-6bce61cabab2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
95eb1a9e-9077-4387-bac7-6bce61cabab2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
95eb1a9e-9077-4387-bac7-6bce61cabab2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
95eb1a9e-9077-4387-bac7-6bce61cabab2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
95eb1a9e-9077-4387-bac7-6bce61cabab2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
95eb1a9e-9077-4387-bac7-6bce61cabab2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
95eb1a9e-9077-4387-bac7-6bce61cabab2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
95eb1a9e-9077-4387-bac7-6bce61cabab2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
95eb1a9e-9077-4387-bac7-6bce61cabab2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
95eb1a9e-9077-4387-bac7-6bce61cabab2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
95eb1a9e-9077-4387-bac7-6bce61cabab2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
95eb1a9e-9077-4387-bac7-6bce61cabab2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
95eb1a9e-9077-4387-bac7-6bce61cabab2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
95eb1a9e-9077-4387-bac7-6bce61cabab2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
95eb1a9e-9077-4387-bac7-6bce61cabab2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
95eb1a9e-9077-4387-bac7-6bce61cabab2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
95eb1a9e-9077-4387-bac7-6bce61cabab2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
28ac1643-95cf-4275-9a8a-6d04242ea841,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Table 1.12: Third-degree block summary.,True,Third-Degree Atrioventricular Block,,,,
137e1f5a-d874-4b96-9c82-6b7aba36d4ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Left Bundle Branch Block,False,Left Bundle Branch Block,,,,
3827ae4f-de2b-426d-882a-1c1eeb13efcc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"A left bundle branch block (LBBB) is generated when the conductivity of the His-Purkinje system in the left ventricle is compromised, either through damage or disease. The ECG changes, and criteria for LBBB relate to these changes in conductivity and the left-side location.",True,Left Bundle Branch Block,,,,
8a2f768d-27b1-4911-ab15-bec80a68e049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8a2f768d-27b1-4911-ab15-bec80a68e049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8a2f768d-27b1-4911-ab15-bec80a68e049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8a2f768d-27b1-4911-ab15-bec80a68e049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8a2f768d-27b1-4911-ab15-bec80a68e049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8a2f768d-27b1-4911-ab15-bec80a68e049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8a2f768d-27b1-4911-ab15-bec80a68e049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8a2f768d-27b1-4911-ab15-bec80a68e049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8a2f768d-27b1-4911-ab15-bec80a68e049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8a2f768d-27b1-4911-ab15-bec80a68e049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8a2f768d-27b1-4911-ab15-bec80a68e049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8a2f768d-27b1-4911-ab15-bec80a68e049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8a2f768d-27b1-4911-ab15-bec80a68e049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8a2f768d-27b1-4911-ab15-bec80a68e049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8a2f768d-27b1-4911-ab15-bec80a68e049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8a2f768d-27b1-4911-ab15-bec80a68e049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8a2f768d-27b1-4911-ab15-bec80a68e049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
27adf2f8-0aeb-490b-acff-1438e7136316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The lateral leads (I, V5, and V6) normally show a downward deflecting Q-wave as normal septal deflection initially occurs left-to-right (i.e., away from the lateral leads). In LBBB the change in direction to right-to-left, plus the longer duration, eliminates the Q-wave from the lateral leads, and Q-waves will be small in aVL.",True,Left Bundle Branch Block,,,,
4b2e83e9-5f9d-48d4-98e8-269f34cc5365,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4b2e83e9-5f9d-48d4-98e8-269f34cc5365,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4b2e83e9-5f9d-48d4-98e8-269f34cc5365,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4b2e83e9-5f9d-48d4-98e8-269f34cc5365,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4b2e83e9-5f9d-48d4-98e8-269f34cc5365,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4b2e83e9-5f9d-48d4-98e8-269f34cc5365,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4b2e83e9-5f9d-48d4-98e8-269f34cc5365,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4b2e83e9-5f9d-48d4-98e8-269f34cc5365,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4b2e83e9-5f9d-48d4-98e8-269f34cc5365,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4b2e83e9-5f9d-48d4-98e8-269f34cc5365,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4b2e83e9-5f9d-48d4-98e8-269f34cc5365,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4b2e83e9-5f9d-48d4-98e8-269f34cc5365,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4b2e83e9-5f9d-48d4-98e8-269f34cc5365,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4b2e83e9-5f9d-48d4-98e8-269f34cc5365,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4b2e83e9-5f9d-48d4-98e8-269f34cc5365,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4b2e83e9-5f9d-48d4-98e8-269f34cc5365,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
4b2e83e9-5f9d-48d4-98e8-269f34cc5365,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
083c72ea-716f-4166-8f90-8ae87b43ec53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
083c72ea-716f-4166-8f90-8ae87b43ec53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
083c72ea-716f-4166-8f90-8ae87b43ec53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
083c72ea-716f-4166-8f90-8ae87b43ec53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
083c72ea-716f-4166-8f90-8ae87b43ec53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
083c72ea-716f-4166-8f90-8ae87b43ec53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
083c72ea-716f-4166-8f90-8ae87b43ec53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
083c72ea-716f-4166-8f90-8ae87b43ec53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
083c72ea-716f-4166-8f90-8ae87b43ec53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
083c72ea-716f-4166-8f90-8ae87b43ec53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
083c72ea-716f-4166-8f90-8ae87b43ec53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
083c72ea-716f-4166-8f90-8ae87b43ec53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
083c72ea-716f-4166-8f90-8ae87b43ec53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
083c72ea-716f-4166-8f90-8ae87b43ec53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
083c72ea-716f-4166-8f90-8ae87b43ec53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
083c72ea-716f-4166-8f90-8ae87b43ec53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
083c72ea-716f-4166-8f90-8ae87b43ec53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
79e52725-ca65-497f-a5bd-9a23f028e22e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Table 1.13: LBBB summary.,True,Left Bundle Branch Block,,,,
ed3f8dde-40ae-4043-a8f4-9694b4a43e97,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Right Bundle Branch Block,False,Right Bundle Branch Block,,,,
fa5f163d-a7ec-4eac-aca1-eb3f0f687df3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The causes and manifestations of a right bundle branch block (RBBB) bear some similarities to those described for LBBB, but of course this time its depolarization of the right ventricle is delayed. Causes of RBBB include ischemic heart disease again as well as other myocardial diseases, but pulmonary issues such as pulmonary embolism and cor pulmonale can be added to the list.",True,Right Bundle Branch Block,,,,
4c6617f5-093a-4400-82a0-1fa211b3e09a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
4c6617f5-093a-4400-82a0-1fa211b3e09a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
4c6617f5-093a-4400-82a0-1fa211b3e09a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
4c6617f5-093a-4400-82a0-1fa211b3e09a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
4c6617f5-093a-4400-82a0-1fa211b3e09a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
4c6617f5-093a-4400-82a0-1fa211b3e09a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
4c6617f5-093a-4400-82a0-1fa211b3e09a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
4c6617f5-093a-4400-82a0-1fa211b3e09a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
4c6617f5-093a-4400-82a0-1fa211b3e09a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
4c6617f5-093a-4400-82a0-1fa211b3e09a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
4c6617f5-093a-4400-82a0-1fa211b3e09a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
4c6617f5-093a-4400-82a0-1fa211b3e09a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
4c6617f5-093a-4400-82a0-1fa211b3e09a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
4c6617f5-093a-4400-82a0-1fa211b3e09a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
4c6617f5-093a-4400-82a0-1fa211b3e09a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
4c6617f5-093a-4400-82a0-1fa211b3e09a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
4c6617f5-093a-4400-82a0-1fa211b3e09a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
001f7f1f-d474-49b0-ae08-1d7679cd5e08,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Table 1.14: RBBB summary.,True,Right Bundle Branch Block,,,,
7e984ecb-ccb6-451f-9dce-51abb9b0b186,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Wolff-Parkinson-White Syndrome,False,Wolff-Parkinson-White Syndrome,,,,
49cb752d-7774-4fd1-b901-0c5c721456e9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Normally the only electrical connection between the atria and the ventricles is the AV node. Otherwise the fibrous skeleton of the heart electrically insulates the atria from the ventricles. In Wolff-Parkinson-White (WPW) syndrome, that insulation is incomplete, and an “accessory pathway” connects the electrical system of the atria directly to the ventricles. If you think of the AV node as a bridge over the fibrous wall with regulated access, the accessory pathway is like a pathological tunnel under it with no regulation.",True,Wolff-Parkinson-White Syndrome,,,,
a915dead-7b62-4635-ab6a-682de3710c45,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
a915dead-7b62-4635-ab6a-682de3710c45,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
a915dead-7b62-4635-ab6a-682de3710c45,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
a915dead-7b62-4635-ab6a-682de3710c45,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
a915dead-7b62-4635-ab6a-682de3710c45,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
a915dead-7b62-4635-ab6a-682de3710c45,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
a915dead-7b62-4635-ab6a-682de3710c45,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
a915dead-7b62-4635-ab6a-682de3710c45,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
a915dead-7b62-4635-ab6a-682de3710c45,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
a915dead-7b62-4635-ab6a-682de3710c45,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
a915dead-7b62-4635-ab6a-682de3710c45,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
a915dead-7b62-4635-ab6a-682de3710c45,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
a915dead-7b62-4635-ab6a-682de3710c45,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
a915dead-7b62-4635-ab6a-682de3710c45,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
a915dead-7b62-4635-ab6a-682de3710c45,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
a915dead-7b62-4635-ab6a-682de3710c45,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
a915dead-7b62-4635-ab6a-682de3710c45,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c5e1b1d4-ec30-4fed-a033-16f9d10a1578,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"WPW syndrome is often asymptomatic, and patients do not require immediate treatment. However, if atrial fibrillation occurs in a WPW patient, the accessory pathway can allow the atrial fibrillation waves through to the ventricle (with no AV nodal refractory period to prevent them). Consequently a high ventricular rate is seen, and the risk of ventricular fibrillation being established means immediate clinical attention is required.",True,Wolff-Parkinson-White Syndrome,,,,
0593bebe-558b-4f03-aadb-b686467f18d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Hyper- and Hypocalcemia,False,Hyper- and Hypocalcemia,,,,
e438fa0f-ea48-41d4-9264-698dbc5700c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e438fa0f-ea48-41d4-9264-698dbc5700c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e438fa0f-ea48-41d4-9264-698dbc5700c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e438fa0f-ea48-41d4-9264-698dbc5700c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e438fa0f-ea48-41d4-9264-698dbc5700c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e438fa0f-ea48-41d4-9264-698dbc5700c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e438fa0f-ea48-41d4-9264-698dbc5700c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e438fa0f-ea48-41d4-9264-698dbc5700c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e438fa0f-ea48-41d4-9264-698dbc5700c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e438fa0f-ea48-41d4-9264-698dbc5700c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e438fa0f-ea48-41d4-9264-698dbc5700c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e438fa0f-ea48-41d4-9264-698dbc5700c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e438fa0f-ea48-41d4-9264-698dbc5700c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e438fa0f-ea48-41d4-9264-698dbc5700c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e438fa0f-ea48-41d4-9264-698dbc5700c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e438fa0f-ea48-41d4-9264-698dbc5700c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e438fa0f-ea48-41d4-9264-698dbc5700c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
61d23ce5-9dcf-4190-973c-00a6a020da0c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
61d23ce5-9dcf-4190-973c-00a6a020da0c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
61d23ce5-9dcf-4190-973c-00a6a020da0c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
61d23ce5-9dcf-4190-973c-00a6a020da0c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
61d23ce5-9dcf-4190-973c-00a6a020da0c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
61d23ce5-9dcf-4190-973c-00a6a020da0c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
61d23ce5-9dcf-4190-973c-00a6a020da0c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
61d23ce5-9dcf-4190-973c-00a6a020da0c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
61d23ce5-9dcf-4190-973c-00a6a020da0c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
61d23ce5-9dcf-4190-973c-00a6a020da0c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
61d23ce5-9dcf-4190-973c-00a6a020da0c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
61d23ce5-9dcf-4190-973c-00a6a020da0c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
61d23ce5-9dcf-4190-973c-00a6a020da0c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
61d23ce5-9dcf-4190-973c-00a6a020da0c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
61d23ce5-9dcf-4190-973c-00a6a020da0c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
61d23ce5-9dcf-4190-973c-00a6a020da0c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
61d23ce5-9dcf-4190-973c-00a6a020da0c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
834f30ec-6400-4e7f-b4d6-ad41cbe94ebe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Table 1.16: Hyper- and hypocalcemia summary.,True,Hyper- and Hypocalcemia,,,,
972c49b8-d64e-4f3b-bd97-58db9d2737c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Hyper- and Hypokalemia,False,Hyper- and Hypokalemia,,,,
dc11f980-5f5f-4f83-a49a-e080901f4b32,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"The pathophysiology is not as simple as changes in extracellular K+ changing the electrochemical gradient for K+. Because of potassium’s role in maintaining the resting membrane potential, shifts in extracellular potassium can also influence the activity of Na+ and Ca++ channels.",True,Hyper- and Hypokalemia,,,,
94360d8d-d05d-466f-b173-91edc50c357f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
94360d8d-d05d-466f-b173-91edc50c357f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
94360d8d-d05d-466f-b173-91edc50c357f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
94360d8d-d05d-466f-b173-91edc50c357f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
94360d8d-d05d-466f-b173-91edc50c357f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
94360d8d-d05d-466f-b173-91edc50c357f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
94360d8d-d05d-466f-b173-91edc50c357f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
94360d8d-d05d-466f-b173-91edc50c357f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
94360d8d-d05d-466f-b173-91edc50c357f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
94360d8d-d05d-466f-b173-91edc50c357f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
94360d8d-d05d-466f-b173-91edc50c357f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
94360d8d-d05d-466f-b173-91edc50c357f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
94360d8d-d05d-466f-b173-91edc50c357f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
94360d8d-d05d-466f-b173-91edc50c357f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
94360d8d-d05d-466f-b173-91edc50c357f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
94360d8d-d05d-466f-b173-91edc50c357f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
94360d8d-d05d-466f-b173-91edc50c357f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
73be44b6-4080-4e9c-bad8-d6aae915fee0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"As hypokalemia also inhibits Na+-K+ ATPase, Na+ accumulates inside the cell. This in turn leads to an accumulation of Ca++ because of a subsequent failure of the Na+-Ca++ exchanger. Extended presence of these two positive ions inside the myocyte prolongs the action potential and may manifest as an increased width and amplitude of the P-wave.",True,Hyper- and Hypokalemia,,,,
f6e8b2fd-0b93-4a1f-84f6-2bf6b8d812b9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"As hypokalemia worsens, the problems with K+ conductance and repolarization increase, and the myocardium becomes susceptible to early after-depolarization (EAD) arrhythmias.",True,Hyper- and Hypokalemia,,,,
32885996-dbcd-4dbe-acc9-201d097a3249,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
32885996-dbcd-4dbe-acc9-201d097a3249,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
32885996-dbcd-4dbe-acc9-201d097a3249,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
32885996-dbcd-4dbe-acc9-201d097a3249,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
32885996-dbcd-4dbe-acc9-201d097a3249,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
32885996-dbcd-4dbe-acc9-201d097a3249,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
32885996-dbcd-4dbe-acc9-201d097a3249,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
32885996-dbcd-4dbe-acc9-201d097a3249,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
32885996-dbcd-4dbe-acc9-201d097a3249,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
32885996-dbcd-4dbe-acc9-201d097a3249,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
32885996-dbcd-4dbe-acc9-201d097a3249,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
32885996-dbcd-4dbe-acc9-201d097a3249,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
32885996-dbcd-4dbe-acc9-201d097a3249,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
32885996-dbcd-4dbe-acc9-201d097a3249,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
32885996-dbcd-4dbe-acc9-201d097a3249,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
32885996-dbcd-4dbe-acc9-201d097a3249,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
32885996-dbcd-4dbe-acc9-201d097a3249,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
0a3e692a-7d5c-4408-b1e2-9be31124fd01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3e692a-7d5c-4408-b1e2-9be31124fd01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3e692a-7d5c-4408-b1e2-9be31124fd01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3e692a-7d5c-4408-b1e2-9be31124fd01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3e692a-7d5c-4408-b1e2-9be31124fd01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3e692a-7d5c-4408-b1e2-9be31124fd01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3e692a-7d5c-4408-b1e2-9be31124fd01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3e692a-7d5c-4408-b1e2-9be31124fd01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3e692a-7d5c-4408-b1e2-9be31124fd01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3e692a-7d5c-4408-b1e2-9be31124fd01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3e692a-7d5c-4408-b1e2-9be31124fd01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3e692a-7d5c-4408-b1e2-9be31124fd01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3e692a-7d5c-4408-b1e2-9be31124fd01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3e692a-7d5c-4408-b1e2-9be31124fd01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3e692a-7d5c-4408-b1e2-9be31124fd01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3e692a-7d5c-4408-b1e2-9be31124fd01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
0a3e692a-7d5c-4408-b1e2-9be31124fd01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
a437b4a5-5abf-48d1-a7b8-1d6cc939e77f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
a437b4a5-5abf-48d1-a7b8-1d6cc939e77f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
a437b4a5-5abf-48d1-a7b8-1d6cc939e77f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
a437b4a5-5abf-48d1-a7b8-1d6cc939e77f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
a437b4a5-5abf-48d1-a7b8-1d6cc939e77f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
a437b4a5-5abf-48d1-a7b8-1d6cc939e77f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
a437b4a5-5abf-48d1-a7b8-1d6cc939e77f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
a437b4a5-5abf-48d1-a7b8-1d6cc939e77f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
a437b4a5-5abf-48d1-a7b8-1d6cc939e77f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
a437b4a5-5abf-48d1-a7b8-1d6cc939e77f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
a437b4a5-5abf-48d1-a7b8-1d6cc939e77f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
a437b4a5-5abf-48d1-a7b8-1d6cc939e77f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
a437b4a5-5abf-48d1-a7b8-1d6cc939e77f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
a437b4a5-5abf-48d1-a7b8-1d6cc939e77f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
a437b4a5-5abf-48d1-a7b8-1d6cc939e77f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
a437b4a5-5abf-48d1-a7b8-1d6cc939e77f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
a437b4a5-5abf-48d1-a7b8-1d6cc939e77f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
082ca810-ee1e-4100-91a1-b168a21f87c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
082ca810-ee1e-4100-91a1-b168a21f87c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
082ca810-ee1e-4100-91a1-b168a21f87c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
082ca810-ee1e-4100-91a1-b168a21f87c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
082ca810-ee1e-4100-91a1-b168a21f87c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
082ca810-ee1e-4100-91a1-b168a21f87c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
082ca810-ee1e-4100-91a1-b168a21f87c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
082ca810-ee1e-4100-91a1-b168a21f87c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
082ca810-ee1e-4100-91a1-b168a21f87c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
082ca810-ee1e-4100-91a1-b168a21f87c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
082ca810-ee1e-4100-91a1-b168a21f87c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
082ca810-ee1e-4100-91a1-b168a21f87c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
082ca810-ee1e-4100-91a1-b168a21f87c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
082ca810-ee1e-4100-91a1-b168a21f87c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
082ca810-ee1e-4100-91a1-b168a21f87c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
082ca810-ee1e-4100-91a1-b168a21f87c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
082ca810-ee1e-4100-91a1-b168a21f87c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
8fdf8615-fbe4-4b40-8c1b-9bb890a5329d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Table 1.17: Hypo- and hyperkalemia summary.,True,Hyper- and Hypokalemia,,,,
40bdc4a2-c962-40b8-8aab-9ab359df9913,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"References, resources, and further reading",False,"References, resources, and further reading",,,,
2c9a0b42-3dff-4148-93dc-634202c7aab6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,Text,False,Text,,,,
4abacb5b-654a-4a98-b086-1a816cc464c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Burns, Ed, and Robert Buttner. Hypercalcaemia. Lift in the Fast Lane, 2021. https://litfl.com/hypercalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
6ff7cfc4-be0d-4fbd-955a-0321ce8cd3b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Burns, Ed, and Robert Buttner. Hypocalcaemia. Life in the Fast Lane, 2021. https://litfl.com/hypocalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
10f24ece-e2a4-4585-aa25-27ba1f47822d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Buttner, Robert, and Ed Burns. Hyperkalaemia. Life in the Fast Lane. https://litfl.com/hyperkalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
26193b31-d598-4b0f-9f5b-2199ea7f9cd2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Buttner, Robert, and Ed Burns. Hypokalaemia. Life in the Fast Lane, 2021. https://litfl.com/hypokalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
4bf9e6e9-ebbf-429e-9926-e0c475858234,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Chhabra, Lovely, Amandeep Goyal, and Michael D. Benham. Wolff Parkinson White Syndrome. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK554437/, CC BY 4.0.",True,Text,,,,
d932ed02-9c09-4da2-942e-396947424482,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Custer, Adam M., Varun S. Yelamanchili, and Sarah L. Lappin. Multifocal Atrial Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459152/, CC BY 4.0.",True,Text,,,,
c1b2ff37-6533-40e9-b2f4-1384927e0382,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Farzam, Khashayar, and John R. Richards. Premature Ventricular Contraction. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532991/, CC BY 4.0.",True,Text,,,,
3cf32402-65f4-43ee-b326-f1817a4a7d17,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Foth, Christopher, Manesh Kumar Gangwani, and Heidi Alvey. Ventricular Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532954/, CC BY 4.0.",True,Text,,,,
550ad85a-9796-4a63-8c33-c38390b6b50c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Hafeez, Yamama, and Shamai A. Grossman. Sinus Bradycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK493201/, CC BY 4.0.",True,Text,,,,
a6e77f7e-332d-430c-8b06-747140df8c0c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Harkness, Weston T., and Mary Hicks. Right Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK507872/, CC BY 4.0.",True,Text,,,,
0daffe50-f016-4845-be73-05b92e26c392,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Heaton, Joseph, and Srikanth Yandrapalli. Premature Atrial Contractions. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK559204/, CC BY 4.0.",True,Text,,,,
47d33957-442e-4566-a733-7b7b7845d237,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Kashou, Anthony H., Amandeep Goyal, Tran Nguyen, and Lovely Chhabra. Atrioventricular Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459147/, CC BY 4.0.",True,Text,,,,
a1b5d160-d70c-4684-abe6-89e919c71b63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,“Learn the Heart.” Healio. https://www.healio.com/cardiology/learn-the-heart.,True,Text,,,,
b103bd91-c715-4c32-b894-d40d6d9b6fb4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Ludhwani, Dipesh, Amandeep Goyal, and Mandar Jagtap. Ventricular Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK537120/, CC BY 4.0.",True,Text,,,,
c37136bd-b976-4f19-baa8-fbd9e173addf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Nesheiwat, Zeid, Amandeep Goyal, and Mandar Jagtap. Atrial Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK526072/, CC BY 4.0.",True,Text,,,,
6a958e57-a7ab-4504-b11c-a811114123ea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Pipilas, Daniel C., Bruce A. Koplan, and Leonard S. Lilly. “The Electrocardiogram.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 4. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
59cdf517-0e19-4df8-b835-a7998672408f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Rodriguez Ziccardi, Mary, Amandeep Goyal, and Christopher V. Maani. Atrial Flutter. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK540985/, CC BY 4.0.",True,Text,,,,
25bb4f13-4d5f-4667-8a7b-2c17e3cebb2f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-10,"Scherbak, Dmitriy, and Gregory J. Hicks. Left Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK482167/, CC BY 4.0.",True,Text,,,,
bc6c29ab-ff65-49ac-be98-9175080164f4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,USMLE,False,USMLE,,,,
a6259fe8-4c87-427f-9927-221c502baefa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
a6259fe8-4c87-427f-9927-221c502baefa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
a6259fe8-4c87-427f-9927-221c502baefa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
a6259fe8-4c87-427f-9927-221c502baefa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
a6259fe8-4c87-427f-9927-221c502baefa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
a6259fe8-4c87-427f-9927-221c502baefa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
a6259fe8-4c87-427f-9927-221c502baefa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
a6259fe8-4c87-427f-9927-221c502baefa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
a6259fe8-4c87-427f-9927-221c502baefa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
a6259fe8-4c87-427f-9927-221c502baefa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
a6259fe8-4c87-427f-9927-221c502baefa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
a6259fe8-4c87-427f-9927-221c502baefa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
a6259fe8-4c87-427f-9927-221c502baefa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
a6259fe8-4c87-427f-9927-221c502baefa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
a6259fe8-4c87-427f-9927-221c502baefa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
a6259fe8-4c87-427f-9927-221c502baefa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
a6259fe8-4c87-427f-9927-221c502baefa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
881292ea-a899-4e23-80fa-8eb16f22b862,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,10q22,False,10q22,,,,
f595d97c-aeda-4c95-bf35-7c3d3681abb0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,q24,False,q24,,,,
e8c92882-6216-4d1e-926c-c7fdbeb1ef23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,fibrillatory,False,fibrillatory,,,,
03cfbdc6-3a1a-42a0-82ba-3bfc0d8f0e63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
03cfbdc6-3a1a-42a0-82ba-3bfc0d8f0e63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
03cfbdc6-3a1a-42a0-82ba-3bfc0d8f0e63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
03cfbdc6-3a1a-42a0-82ba-3bfc0d8f0e63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
03cfbdc6-3a1a-42a0-82ba-3bfc0d8f0e63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
03cfbdc6-3a1a-42a0-82ba-3bfc0d8f0e63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
03cfbdc6-3a1a-42a0-82ba-3bfc0d8f0e63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
03cfbdc6-3a1a-42a0-82ba-3bfc0d8f0e63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
03cfbdc6-3a1a-42a0-82ba-3bfc0d8f0e63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
03cfbdc6-3a1a-42a0-82ba-3bfc0d8f0e63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
03cfbdc6-3a1a-42a0-82ba-3bfc0d8f0e63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
03cfbdc6-3a1a-42a0-82ba-3bfc0d8f0e63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
03cfbdc6-3a1a-42a0-82ba-3bfc0d8f0e63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
03cfbdc6-3a1a-42a0-82ba-3bfc0d8f0e63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
03cfbdc6-3a1a-42a0-82ba-3bfc0d8f0e63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
03cfbdc6-3a1a-42a0-82ba-3bfc0d8f0e63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
03cfbdc6-3a1a-42a0-82ba-3bfc0d8f0e63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
19ef7111-77a9-4f02-89c6-960f7a51e317,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Table 1.1: Atrial fibrillation summary.,True,fibrillatory,,,,
373d6e2d-8b8f-4d1c-90a8-621b8a9588f2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Atrial Flutter,False,Atrial Flutter,,,,
cde2a8c2-4f2a-4980-91c2-54b60fef9f39,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
cde2a8c2-4f2a-4980-91c2-54b60fef9f39,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
cde2a8c2-4f2a-4980-91c2-54b60fef9f39,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
cde2a8c2-4f2a-4980-91c2-54b60fef9f39,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
cde2a8c2-4f2a-4980-91c2-54b60fef9f39,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
cde2a8c2-4f2a-4980-91c2-54b60fef9f39,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
cde2a8c2-4f2a-4980-91c2-54b60fef9f39,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
cde2a8c2-4f2a-4980-91c2-54b60fef9f39,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
cde2a8c2-4f2a-4980-91c2-54b60fef9f39,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
cde2a8c2-4f2a-4980-91c2-54b60fef9f39,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
cde2a8c2-4f2a-4980-91c2-54b60fef9f39,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
cde2a8c2-4f2a-4980-91c2-54b60fef9f39,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
cde2a8c2-4f2a-4980-91c2-54b60fef9f39,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
cde2a8c2-4f2a-4980-91c2-54b60fef9f39,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
cde2a8c2-4f2a-4980-91c2-54b60fef9f39,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
cde2a8c2-4f2a-4980-91c2-54b60fef9f39,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
cde2a8c2-4f2a-4980-91c2-54b60fef9f39,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
53c4dfc9-60af-4f98-812b-3d3f3c020bb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,macroreentrant,False,macroreentrant,,,,
431c40d2-1477-4182-bc61-1216d09968e6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,cavotricuspid,False,cavotricuspid,,,,
e59ff7ea-d871-4eef-b29f-ac8c4ad79fe3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"As with atrial fibrillation, the AV node’s refractory period prevents most of the P-waves from progressing to the ventricle, but commonly the AV conduction will be 2-to-1, so with an atrial rate of 300 bpm the ventricular rate will be 150 bpm. Parasympathetic stimulation or changes in AV node refractoriness can modify how many P-waves pass into the ventricle, but the the resultant rhythm is “regularly irregular.” When the heart rate is elevated, then distinguishing flutter from fibrillation becomes challenging and slowing ventricular rate pharmaceutically (adenosine) helps the flutter waves reemerge for a definitive diagnosis to be made.",True,cavotricuspid,,,,
f7acc8cf-9f59-4e8d-9e96-adfdda66dea3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Table 1.2: Atrial flutter summary.,True,cavotricuspid,,,,
f4976d5d-c641-47a0-8d93-121adc58d4ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Multifocal Atrial Tachycardia,False,Multifocal Atrial Tachycardia,,,,
c793abc1-6cff-46e1-9264-38c960492eb6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c793abc1-6cff-46e1-9264-38c960492eb6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c793abc1-6cff-46e1-9264-38c960492eb6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c793abc1-6cff-46e1-9264-38c960492eb6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c793abc1-6cff-46e1-9264-38c960492eb6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c793abc1-6cff-46e1-9264-38c960492eb6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c793abc1-6cff-46e1-9264-38c960492eb6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c793abc1-6cff-46e1-9264-38c960492eb6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c793abc1-6cff-46e1-9264-38c960492eb6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c793abc1-6cff-46e1-9264-38c960492eb6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c793abc1-6cff-46e1-9264-38c960492eb6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c793abc1-6cff-46e1-9264-38c960492eb6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c793abc1-6cff-46e1-9264-38c960492eb6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c793abc1-6cff-46e1-9264-38c960492eb6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c793abc1-6cff-46e1-9264-38c960492eb6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c793abc1-6cff-46e1-9264-38c960492eb6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
c793abc1-6cff-46e1-9264-38c960492eb6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
68fbd13f-b80c-45f4-ac4d-d065e12a374b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"MAT frequently occurs in the setting of severe lung disease and, more specifically, during an exacerbation of lung disease. This rhythm is benign, and once the underlying lung disease is treated, it should resolve.",True,Multifocal Atrial Tachycardia,,,,
3fc9ac09-a330-4f51-8ece-ce76d5eccc14,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Table 1.3: MAT summary.,True,Multifocal Atrial Tachycardia,,,,
036368ad-c382-4e0e-81c9-b41813d6d2a0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Premature Atrial Contraction,False,Premature Atrial Contraction,,,,
43c247eb-62b5-42f5-9c6d-3d795c8852e0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A premature atrial contraction (PAC) is generated by a depolarization instigated outside of the SA node. This produces an extra P-wave, and consequently a shortening from previous P-P intervals is seen. The aberrant P-wave also has a different morphology from a sinus P-wave because of its different anatomical origin.",True,Premature Atrial Contraction,,,,
8a46aae3-da16-4129-bdbf-6d562ca1328a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
8a46aae3-da16-4129-bdbf-6d562ca1328a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
8a46aae3-da16-4129-bdbf-6d562ca1328a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
8a46aae3-da16-4129-bdbf-6d562ca1328a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
8a46aae3-da16-4129-bdbf-6d562ca1328a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
8a46aae3-da16-4129-bdbf-6d562ca1328a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
8a46aae3-da16-4129-bdbf-6d562ca1328a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
8a46aae3-da16-4129-bdbf-6d562ca1328a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
8a46aae3-da16-4129-bdbf-6d562ca1328a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
8a46aae3-da16-4129-bdbf-6d562ca1328a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
8a46aae3-da16-4129-bdbf-6d562ca1328a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
8a46aae3-da16-4129-bdbf-6d562ca1328a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
8a46aae3-da16-4129-bdbf-6d562ca1328a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
8a46aae3-da16-4129-bdbf-6d562ca1328a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
8a46aae3-da16-4129-bdbf-6d562ca1328a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
8a46aae3-da16-4129-bdbf-6d562ca1328a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
8a46aae3-da16-4129-bdbf-6d562ca1328a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
4a277ca8-1b34-4e18-9b31-c525679aa45d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"If a PAC occurs when the AV node has not yet recovered from its refractory period, the PAC will fail to conduct to the ventricles; meaning the PAC will not be followed by a QRS complex or the ectopic P-R interval will be prolonged. The ECG will show a premature, ectopic P-wave and then no QRS complex afterward. When this occurs along with bigeminy, the ECG can appear as if there is sinus bradycardia.",True,Premature Atrial Contraction,,,,
80dfcf08-3bbb-42ce-8c24-a1904d779548,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Table 1.4: PAC summary.,True,Premature Atrial Contraction,,,,
a0c68e79-144b-414f-810b-bd9886f42999,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Sinus Bradycardia,False,Sinus Bradycardia,,,,
13b5fe69-c703-4115-853b-44d1c314158d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Sinus bradycardia denotes a sinus rhythm below 60 bpm. Otherwise the ECG waveform is normal on an ECG with an upright P-wave in lead II preceding every QRS complex. There are many intrinsic causes associated with the heart itself, as well as extrinsic causes, some of which are listed table 1.5. Sinus bradycardia is usually asymptomatic as rates of 40–50 bpm can maintain hemodynamic stability. Rates below this can produce symptoms of fatigue, dizziness, and dyspnea on exertion.",True,Sinus Bradycardia,,,,
9d50e948-de49-4df5-ad45-3ff96c67ee8d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Table 1.5: Intrinsic and extrinsic causes associated with the heart.,True,Sinus Bradycardia,,,,
a5ff892e-e7d1-46bd-85d0-1acb98cb60f9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Table 1.6: Sinus bradycardia summary.,True,Sinus Bradycardia,,,,
5fbd9d62-3be5-4e33-ae51-dd85482a8e37,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Premature Ventricular Contractions,False,Premature Ventricular Contractions,,,,
7caf581c-e815-4690-a39a-a76ba9aacb57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
7caf581c-e815-4690-a39a-a76ba9aacb57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
7caf581c-e815-4690-a39a-a76ba9aacb57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
7caf581c-e815-4690-a39a-a76ba9aacb57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
7caf581c-e815-4690-a39a-a76ba9aacb57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
7caf581c-e815-4690-a39a-a76ba9aacb57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
7caf581c-e815-4690-a39a-a76ba9aacb57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
7caf581c-e815-4690-a39a-a76ba9aacb57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
7caf581c-e815-4690-a39a-a76ba9aacb57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
7caf581c-e815-4690-a39a-a76ba9aacb57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
7caf581c-e815-4690-a39a-a76ba9aacb57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
7caf581c-e815-4690-a39a-a76ba9aacb57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
7caf581c-e815-4690-a39a-a76ba9aacb57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
7caf581c-e815-4690-a39a-a76ba9aacb57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
7caf581c-e815-4690-a39a-a76ba9aacb57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
7caf581c-e815-4690-a39a-a76ba9aacb57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
7caf581c-e815-4690-a39a-a76ba9aacb57,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
e1de7e7e-4c90-4482-9f7f-17a8e9a296eb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Table 1.7: PVC summary.,True,Premature Ventricular Contractions,,,,
d7e0002c-e90c-4f27-ad34-bba9572b9426,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Ventricular Tachycardia,False,Ventricular Tachycardia,,,,
55057f3d-8bab-43a2-a309-cdf436017dba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Ventricular tachycardia (VT) is caused by reentry currents being established in the ventricular myocardium or groups of ventricular myocytes that have aberrant electrical behavior. As such, VT is usually caused by underlying cardiac disease.",True,Ventricular Tachycardia,,,,
a962823d-ce1b-4e82-bc84-842f2df0a0d7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Like a PVC, the aberrant depolarizations do not follow the normal conduction pathways so are wide (>120 msecs), but unlike a PVC, VT involves a ventricular rate >100 bpm. With disorganized contractility and reduced filling time, VT can lead to hemodynamic instability and severe hypotension—hence it is life threatening.",True,Ventricular Tachycardia,,,,
e5a56fd1-dd83-4924-bc8c-5a2b32e53ed4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The QRS morphology in VT is highly variable between patients and depends on where the arrhythmia originates. Consequently there are several ways to classify VT based on duration, symptoms, QRS morphology, rate, and origin.",True,Ventricular Tachycardia,,,,
0077e6b9-4d8f-42e9-b67b-a7e67e447cfb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Sustained VT is any VT that lasts for more than 30 seconds or is symptomatic. Nonsustained VT lasts for less than 30 seconds and is asymptomatic.,True,Ventricular Tachycardia,,,,
c7e384ea-62f3-48ff-af32-a9e0e3765d79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
c7e384ea-62f3-48ff-af32-a9e0e3765d79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
c7e384ea-62f3-48ff-af32-a9e0e3765d79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
c7e384ea-62f3-48ff-af32-a9e0e3765d79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
c7e384ea-62f3-48ff-af32-a9e0e3765d79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
c7e384ea-62f3-48ff-af32-a9e0e3765d79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
c7e384ea-62f3-48ff-af32-a9e0e3765d79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
c7e384ea-62f3-48ff-af32-a9e0e3765d79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
c7e384ea-62f3-48ff-af32-a9e0e3765d79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
c7e384ea-62f3-48ff-af32-a9e0e3765d79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
c7e384ea-62f3-48ff-af32-a9e0e3765d79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
c7e384ea-62f3-48ff-af32-a9e0e3765d79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
c7e384ea-62f3-48ff-af32-a9e0e3765d79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
c7e384ea-62f3-48ff-af32-a9e0e3765d79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
c7e384ea-62f3-48ff-af32-a9e0e3765d79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
c7e384ea-62f3-48ff-af32-a9e0e3765d79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
c7e384ea-62f3-48ff-af32-a9e0e3765d79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
81eff418-f15d-42c7-9808-b0d213b5778a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
81eff418-f15d-42c7-9808-b0d213b5778a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
81eff418-f15d-42c7-9808-b0d213b5778a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
81eff418-f15d-42c7-9808-b0d213b5778a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
81eff418-f15d-42c7-9808-b0d213b5778a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
81eff418-f15d-42c7-9808-b0d213b5778a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
81eff418-f15d-42c7-9808-b0d213b5778a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
81eff418-f15d-42c7-9808-b0d213b5778a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
81eff418-f15d-42c7-9808-b0d213b5778a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
81eff418-f15d-42c7-9808-b0d213b5778a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
81eff418-f15d-42c7-9808-b0d213b5778a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
81eff418-f15d-42c7-9808-b0d213b5778a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
81eff418-f15d-42c7-9808-b0d213b5778a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
81eff418-f15d-42c7-9808-b0d213b5778a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
81eff418-f15d-42c7-9808-b0d213b5778a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
81eff418-f15d-42c7-9808-b0d213b5778a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
81eff418-f15d-42c7-9808-b0d213b5778a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
77a95c5b-197f-42e8-9bd5-405d81b385ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Torsades de pointes is associated with a prolonged QT interval (>600 msecs) that helps distinguish it from other forms of polymorphous VT. The longer QT interval can be caused by ionic abnormalities that reduce the repolarizing current of Phase 3 of the cardiac action potential. This makes the myocardium susceptible to early after-depolarizations—the trigger for torsades de pointes. These after-depolarizations do not happen uniformly across the myocardium and are more common in endocardial tissue where the repolarization currents are slower. So torsades de pointes arises from the after-depolarizations causing reentry currents in neighboring tissue.,True,Ventricular Tachycardia,,,,
db558f4f-a5c9-4c17-9269-36b73279c54c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Both common garden variety VTs and torsades de pointes can progress to ventricular fibrillation.,True,Ventricular Tachycardia,,,,
f2f67581-8e91-4231-8abc-17e75ead6f03,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Table 1.8: VT summary.,True,Ventricular Tachycardia,,,,
26e8120c-8f31-453b-953c-ad2d7015bf14,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Ventricular Fibrillation,False,Ventricular Fibrillation,,,,
7320ee92-753a-44cb-96c5-a322bbcf04a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Ventricular fibrillation (VF) occurs when the ventricular rate exceeds 400 bpm. The disorganized and uncoordinated contraction of the myocardium causes cardiac output to fall to catastrophic levels. Rates of survival for out-of-hospital VF are low.,True,Ventricular Fibrillation,,,,
3869be21-a266-4534-bee3-33b42cdf59b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3869be21-a266-4534-bee3-33b42cdf59b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3869be21-a266-4534-bee3-33b42cdf59b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3869be21-a266-4534-bee3-33b42cdf59b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3869be21-a266-4534-bee3-33b42cdf59b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3869be21-a266-4534-bee3-33b42cdf59b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3869be21-a266-4534-bee3-33b42cdf59b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3869be21-a266-4534-bee3-33b42cdf59b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3869be21-a266-4534-bee3-33b42cdf59b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3869be21-a266-4534-bee3-33b42cdf59b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3869be21-a266-4534-bee3-33b42cdf59b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3869be21-a266-4534-bee3-33b42cdf59b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3869be21-a266-4534-bee3-33b42cdf59b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3869be21-a266-4534-bee3-33b42cdf59b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3869be21-a266-4534-bee3-33b42cdf59b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3869be21-a266-4534-bee3-33b42cdf59b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3869be21-a266-4534-bee3-33b42cdf59b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
2e1b9c35-44d0-4e9b-88e0-d53e427339ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Table 1.9: VF summary.,True,Ventricular Fibrillation,,,,
bb63c830-e3e6-4c7a-b8fe-9a4ce1affd87,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,First-Degree Atrioventricular Block,False,First-Degree Atrioventricular Block,,,,
60c05a12-64f7-4e14-b1ca-e50cc01c81c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
60c05a12-64f7-4e14-b1ca-e50cc01c81c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
60c05a12-64f7-4e14-b1ca-e50cc01c81c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
60c05a12-64f7-4e14-b1ca-e50cc01c81c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
60c05a12-64f7-4e14-b1ca-e50cc01c81c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
60c05a12-64f7-4e14-b1ca-e50cc01c81c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
60c05a12-64f7-4e14-b1ca-e50cc01c81c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
60c05a12-64f7-4e14-b1ca-e50cc01c81c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
60c05a12-64f7-4e14-b1ca-e50cc01c81c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
60c05a12-64f7-4e14-b1ca-e50cc01c81c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
60c05a12-64f7-4e14-b1ca-e50cc01c81c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
60c05a12-64f7-4e14-b1ca-e50cc01c81c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
60c05a12-64f7-4e14-b1ca-e50cc01c81c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
60c05a12-64f7-4e14-b1ca-e50cc01c81c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
60c05a12-64f7-4e14-b1ca-e50cc01c81c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
60c05a12-64f7-4e14-b1ca-e50cc01c81c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
60c05a12-64f7-4e14-b1ca-e50cc01c81c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1b4500ce-0606-44b9-ba47-f5ba6950d6b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1b4500ce-0606-44b9-ba47-f5ba6950d6b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1b4500ce-0606-44b9-ba47-f5ba6950d6b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1b4500ce-0606-44b9-ba47-f5ba6950d6b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1b4500ce-0606-44b9-ba47-f5ba6950d6b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1b4500ce-0606-44b9-ba47-f5ba6950d6b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1b4500ce-0606-44b9-ba47-f5ba6950d6b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1b4500ce-0606-44b9-ba47-f5ba6950d6b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1b4500ce-0606-44b9-ba47-f5ba6950d6b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1b4500ce-0606-44b9-ba47-f5ba6950d6b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1b4500ce-0606-44b9-ba47-f5ba6950d6b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1b4500ce-0606-44b9-ba47-f5ba6950d6b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1b4500ce-0606-44b9-ba47-f5ba6950d6b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1b4500ce-0606-44b9-ba47-f5ba6950d6b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1b4500ce-0606-44b9-ba47-f5ba6950d6b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1b4500ce-0606-44b9-ba47-f5ba6950d6b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1b4500ce-0606-44b9-ba47-f5ba6950d6b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
7a82ead5-fa4b-4073-9675-d6994993c827,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Table 1.10: First-degree block summary.,True,First-Degree Atrioventricular Block,,,,
2a7bba41-966a-4d87-8dec-49a4f871090e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Second-Degree Atrioventricular Block,False,Second-Degree Atrioventricular Block,,,,
27d9e997-c711-4d3b-8cfb-3297eb843a46,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A second-degree atrioventricular block also has changes in P-R interval, but it starts to show failure of the P-wave to propagate a QRS complex every time (i.e., intermittently the depolarization fails to reach the ventricles). The pattern of missed ventricular depolarizations, or blocked P-waves, is often very regular and described as a ratio of P-waves to QRS complex. The way in which the P-R interval changes in relation to the blocked P-waves produces subclassifications of second-degree blocks, Mobitz I and II.",True,Second-Degree Atrioventricular Block,,,,
c98ecad3-b308-4e5c-8e14-62fb5d4b77f8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
c98ecad3-b308-4e5c-8e14-62fb5d4b77f8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
c98ecad3-b308-4e5c-8e14-62fb5d4b77f8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
c98ecad3-b308-4e5c-8e14-62fb5d4b77f8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
c98ecad3-b308-4e5c-8e14-62fb5d4b77f8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
c98ecad3-b308-4e5c-8e14-62fb5d4b77f8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
c98ecad3-b308-4e5c-8e14-62fb5d4b77f8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
c98ecad3-b308-4e5c-8e14-62fb5d4b77f8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
c98ecad3-b308-4e5c-8e14-62fb5d4b77f8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
c98ecad3-b308-4e5c-8e14-62fb5d4b77f8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
c98ecad3-b308-4e5c-8e14-62fb5d4b77f8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
c98ecad3-b308-4e5c-8e14-62fb5d4b77f8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
c98ecad3-b308-4e5c-8e14-62fb5d4b77f8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
c98ecad3-b308-4e5c-8e14-62fb5d4b77f8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
c98ecad3-b308-4e5c-8e14-62fb5d4b77f8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
c98ecad3-b308-4e5c-8e14-62fb5d4b77f8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
c98ecad3-b308-4e5c-8e14-62fb5d4b77f8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
2c569dfd-fd6e-48e5-b997-f2106ffd5bf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
2c569dfd-fd6e-48e5-b997-f2106ffd5bf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
2c569dfd-fd6e-48e5-b997-f2106ffd5bf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
2c569dfd-fd6e-48e5-b997-f2106ffd5bf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
2c569dfd-fd6e-48e5-b997-f2106ffd5bf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
2c569dfd-fd6e-48e5-b997-f2106ffd5bf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
2c569dfd-fd6e-48e5-b997-f2106ffd5bf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
2c569dfd-fd6e-48e5-b997-f2106ffd5bf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
2c569dfd-fd6e-48e5-b997-f2106ffd5bf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
2c569dfd-fd6e-48e5-b997-f2106ffd5bf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
2c569dfd-fd6e-48e5-b997-f2106ffd5bf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
2c569dfd-fd6e-48e5-b997-f2106ffd5bf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
2c569dfd-fd6e-48e5-b997-f2106ffd5bf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
2c569dfd-fd6e-48e5-b997-f2106ffd5bf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
2c569dfd-fd6e-48e5-b997-f2106ffd5bf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
2c569dfd-fd6e-48e5-b997-f2106ffd5bf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
2c569dfd-fd6e-48e5-b997-f2106ffd5bf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
45493f54-e823-4df7-9c6b-945e2a6e6f8b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Table 1.11: Second-degree block summary.,True,Second-Degree Atrioventricular Block,,,,
5c7165e1-7946-405f-be74-f7bffe83b143,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Third-Degree Atrioventricular Block,False,Third-Degree Atrioventricular Block,,,,
8c031ee6-9259-4351-85b7-e9c4db54f5e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8c031ee6-9259-4351-85b7-e9c4db54f5e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8c031ee6-9259-4351-85b7-e9c4db54f5e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8c031ee6-9259-4351-85b7-e9c4db54f5e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8c031ee6-9259-4351-85b7-e9c4db54f5e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8c031ee6-9259-4351-85b7-e9c4db54f5e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8c031ee6-9259-4351-85b7-e9c4db54f5e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8c031ee6-9259-4351-85b7-e9c4db54f5e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8c031ee6-9259-4351-85b7-e9c4db54f5e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8c031ee6-9259-4351-85b7-e9c4db54f5e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8c031ee6-9259-4351-85b7-e9c4db54f5e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8c031ee6-9259-4351-85b7-e9c4db54f5e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8c031ee6-9259-4351-85b7-e9c4db54f5e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8c031ee6-9259-4351-85b7-e9c4db54f5e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8c031ee6-9259-4351-85b7-e9c4db54f5e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8c031ee6-9259-4351-85b7-e9c4db54f5e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8c031ee6-9259-4351-85b7-e9c4db54f5e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
bba65017-cc21-430a-b569-b5e967965cb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Table 1.12: Third-degree block summary.,True,Third-Degree Atrioventricular Block,,,,
9833cce4-2088-4329-a576-bc59bab0f069,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Left Bundle Branch Block,False,Left Bundle Branch Block,,,,
a1c835f3-b221-444e-91a1-2dfae609f937,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"A left bundle branch block (LBBB) is generated when the conductivity of the His-Purkinje system in the left ventricle is compromised, either through damage or disease. The ECG changes, and criteria for LBBB relate to these changes in conductivity and the left-side location.",True,Left Bundle Branch Block,,,,
5964f0dd-7ce6-414a-8492-969c8fc433d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5964f0dd-7ce6-414a-8492-969c8fc433d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5964f0dd-7ce6-414a-8492-969c8fc433d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5964f0dd-7ce6-414a-8492-969c8fc433d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5964f0dd-7ce6-414a-8492-969c8fc433d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5964f0dd-7ce6-414a-8492-969c8fc433d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5964f0dd-7ce6-414a-8492-969c8fc433d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5964f0dd-7ce6-414a-8492-969c8fc433d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5964f0dd-7ce6-414a-8492-969c8fc433d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5964f0dd-7ce6-414a-8492-969c8fc433d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5964f0dd-7ce6-414a-8492-969c8fc433d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5964f0dd-7ce6-414a-8492-969c8fc433d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5964f0dd-7ce6-414a-8492-969c8fc433d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5964f0dd-7ce6-414a-8492-969c8fc433d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5964f0dd-7ce6-414a-8492-969c8fc433d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5964f0dd-7ce6-414a-8492-969c8fc433d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
5964f0dd-7ce6-414a-8492-969c8fc433d6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
45e9de27-7217-41ad-a020-9f68b3b8d7f2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The lateral leads (I, V5, and V6) normally show a downward deflecting Q-wave as normal septal deflection initially occurs left-to-right (i.e., away from the lateral leads). In LBBB the change in direction to right-to-left, plus the longer duration, eliminates the Q-wave from the lateral leads, and Q-waves will be small in aVL.",True,Left Bundle Branch Block,,,,
f95cacec-4f33-4f18-83d7-8e25c9db11c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f95cacec-4f33-4f18-83d7-8e25c9db11c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f95cacec-4f33-4f18-83d7-8e25c9db11c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f95cacec-4f33-4f18-83d7-8e25c9db11c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f95cacec-4f33-4f18-83d7-8e25c9db11c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f95cacec-4f33-4f18-83d7-8e25c9db11c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f95cacec-4f33-4f18-83d7-8e25c9db11c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f95cacec-4f33-4f18-83d7-8e25c9db11c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f95cacec-4f33-4f18-83d7-8e25c9db11c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f95cacec-4f33-4f18-83d7-8e25c9db11c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f95cacec-4f33-4f18-83d7-8e25c9db11c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f95cacec-4f33-4f18-83d7-8e25c9db11c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f95cacec-4f33-4f18-83d7-8e25c9db11c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f95cacec-4f33-4f18-83d7-8e25c9db11c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f95cacec-4f33-4f18-83d7-8e25c9db11c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f95cacec-4f33-4f18-83d7-8e25c9db11c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f95cacec-4f33-4f18-83d7-8e25c9db11c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
c0690f3f-64bf-4da9-8e2b-a89e104379d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c0690f3f-64bf-4da9-8e2b-a89e104379d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c0690f3f-64bf-4da9-8e2b-a89e104379d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c0690f3f-64bf-4da9-8e2b-a89e104379d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c0690f3f-64bf-4da9-8e2b-a89e104379d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c0690f3f-64bf-4da9-8e2b-a89e104379d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c0690f3f-64bf-4da9-8e2b-a89e104379d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c0690f3f-64bf-4da9-8e2b-a89e104379d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c0690f3f-64bf-4da9-8e2b-a89e104379d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c0690f3f-64bf-4da9-8e2b-a89e104379d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c0690f3f-64bf-4da9-8e2b-a89e104379d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c0690f3f-64bf-4da9-8e2b-a89e104379d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c0690f3f-64bf-4da9-8e2b-a89e104379d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c0690f3f-64bf-4da9-8e2b-a89e104379d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c0690f3f-64bf-4da9-8e2b-a89e104379d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c0690f3f-64bf-4da9-8e2b-a89e104379d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c0690f3f-64bf-4da9-8e2b-a89e104379d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
12e8d4a3-9f8e-4321-91c6-734317b89676,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Table 1.13: LBBB summary.,True,Left Bundle Branch Block,,,,
18632c8d-907a-4438-944c-feb07dff0c47,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Right Bundle Branch Block,False,Right Bundle Branch Block,,,,
9b17ce90-46c5-4ebc-adaf-1294c13a5984,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The causes and manifestations of a right bundle branch block (RBBB) bear some similarities to those described for LBBB, but of course this time its depolarization of the right ventricle is delayed. Causes of RBBB include ischemic heart disease again as well as other myocardial diseases, but pulmonary issues such as pulmonary embolism and cor pulmonale can be added to the list.",True,Right Bundle Branch Block,,,,
aceabf9a-7ac2-45f7-af79-4daa85865daa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
aceabf9a-7ac2-45f7-af79-4daa85865daa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
aceabf9a-7ac2-45f7-af79-4daa85865daa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
aceabf9a-7ac2-45f7-af79-4daa85865daa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
aceabf9a-7ac2-45f7-af79-4daa85865daa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
aceabf9a-7ac2-45f7-af79-4daa85865daa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
aceabf9a-7ac2-45f7-af79-4daa85865daa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
aceabf9a-7ac2-45f7-af79-4daa85865daa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
aceabf9a-7ac2-45f7-af79-4daa85865daa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
aceabf9a-7ac2-45f7-af79-4daa85865daa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
aceabf9a-7ac2-45f7-af79-4daa85865daa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
aceabf9a-7ac2-45f7-af79-4daa85865daa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
aceabf9a-7ac2-45f7-af79-4daa85865daa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
aceabf9a-7ac2-45f7-af79-4daa85865daa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
aceabf9a-7ac2-45f7-af79-4daa85865daa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
aceabf9a-7ac2-45f7-af79-4daa85865daa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
aceabf9a-7ac2-45f7-af79-4daa85865daa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
9ef43af0-9b2a-4cac-b78e-743f8b793507,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Table 1.14: RBBB summary.,True,Right Bundle Branch Block,,,,
a17aabee-e712-46e8-ae11-d0b934b1c41f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Wolff-Parkinson-White Syndrome,False,Wolff-Parkinson-White Syndrome,,,,
becf8dad-dfd5-42d1-88c4-b3b437c04782,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Normally the only electrical connection between the atria and the ventricles is the AV node. Otherwise the fibrous skeleton of the heart electrically insulates the atria from the ventricles. In Wolff-Parkinson-White (WPW) syndrome, that insulation is incomplete, and an “accessory pathway” connects the electrical system of the atria directly to the ventricles. If you think of the AV node as a bridge over the fibrous wall with regulated access, the accessory pathway is like a pathological tunnel under it with no regulation.",True,Wolff-Parkinson-White Syndrome,,,,
41704972-3a83-4b76-9899-25a34ea50d5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41704972-3a83-4b76-9899-25a34ea50d5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41704972-3a83-4b76-9899-25a34ea50d5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41704972-3a83-4b76-9899-25a34ea50d5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41704972-3a83-4b76-9899-25a34ea50d5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41704972-3a83-4b76-9899-25a34ea50d5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41704972-3a83-4b76-9899-25a34ea50d5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41704972-3a83-4b76-9899-25a34ea50d5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41704972-3a83-4b76-9899-25a34ea50d5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41704972-3a83-4b76-9899-25a34ea50d5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41704972-3a83-4b76-9899-25a34ea50d5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41704972-3a83-4b76-9899-25a34ea50d5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41704972-3a83-4b76-9899-25a34ea50d5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41704972-3a83-4b76-9899-25a34ea50d5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41704972-3a83-4b76-9899-25a34ea50d5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41704972-3a83-4b76-9899-25a34ea50d5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
41704972-3a83-4b76-9899-25a34ea50d5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
a38c325a-2ec5-465e-a014-f9319a4fa0d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"WPW syndrome is often asymptomatic, and patients do not require immediate treatment. However, if atrial fibrillation occurs in a WPW patient, the accessory pathway can allow the atrial fibrillation waves through to the ventricle (with no AV nodal refractory period to prevent them). Consequently a high ventricular rate is seen, and the risk of ventricular fibrillation being established means immediate clinical attention is required.",True,Wolff-Parkinson-White Syndrome,,,,
64d7db55-6025-4c4a-9562-3712c9fb8c3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Hyper- and Hypocalcemia,False,Hyper- and Hypocalcemia,,,,
66403104-217d-4b56-b099-85be9aa86c26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
66403104-217d-4b56-b099-85be9aa86c26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
66403104-217d-4b56-b099-85be9aa86c26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
66403104-217d-4b56-b099-85be9aa86c26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
66403104-217d-4b56-b099-85be9aa86c26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
66403104-217d-4b56-b099-85be9aa86c26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
66403104-217d-4b56-b099-85be9aa86c26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
66403104-217d-4b56-b099-85be9aa86c26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
66403104-217d-4b56-b099-85be9aa86c26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
66403104-217d-4b56-b099-85be9aa86c26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
66403104-217d-4b56-b099-85be9aa86c26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
66403104-217d-4b56-b099-85be9aa86c26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
66403104-217d-4b56-b099-85be9aa86c26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
66403104-217d-4b56-b099-85be9aa86c26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
66403104-217d-4b56-b099-85be9aa86c26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
66403104-217d-4b56-b099-85be9aa86c26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
66403104-217d-4b56-b099-85be9aa86c26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
2351852b-5071-4a8c-ad7c-1f3e8a027727,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
2351852b-5071-4a8c-ad7c-1f3e8a027727,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
2351852b-5071-4a8c-ad7c-1f3e8a027727,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
2351852b-5071-4a8c-ad7c-1f3e8a027727,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
2351852b-5071-4a8c-ad7c-1f3e8a027727,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
2351852b-5071-4a8c-ad7c-1f3e8a027727,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
2351852b-5071-4a8c-ad7c-1f3e8a027727,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
2351852b-5071-4a8c-ad7c-1f3e8a027727,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
2351852b-5071-4a8c-ad7c-1f3e8a027727,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
2351852b-5071-4a8c-ad7c-1f3e8a027727,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
2351852b-5071-4a8c-ad7c-1f3e8a027727,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
2351852b-5071-4a8c-ad7c-1f3e8a027727,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
2351852b-5071-4a8c-ad7c-1f3e8a027727,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
2351852b-5071-4a8c-ad7c-1f3e8a027727,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
2351852b-5071-4a8c-ad7c-1f3e8a027727,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
2351852b-5071-4a8c-ad7c-1f3e8a027727,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
2351852b-5071-4a8c-ad7c-1f3e8a027727,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
a12d2db9-7172-435b-883c-d1182bc97cd3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Table 1.16: Hyper- and hypocalcemia summary.,True,Hyper- and Hypocalcemia,,,,
8452979b-9b98-47c1-900e-650f171a85b9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Hyper- and Hypokalemia,False,Hyper- and Hypokalemia,,,,
f6c7cb63-46a2-4fd8-9303-9ef23de76bb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"The pathophysiology is not as simple as changes in extracellular K+ changing the electrochemical gradient for K+. Because of potassium’s role in maintaining the resting membrane potential, shifts in extracellular potassium can also influence the activity of Na+ and Ca++ channels.",True,Hyper- and Hypokalemia,,,,
7a7a8e27-621f-4e3b-be96-a0f7b01f7642,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
7a7a8e27-621f-4e3b-be96-a0f7b01f7642,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
7a7a8e27-621f-4e3b-be96-a0f7b01f7642,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
7a7a8e27-621f-4e3b-be96-a0f7b01f7642,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
7a7a8e27-621f-4e3b-be96-a0f7b01f7642,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
7a7a8e27-621f-4e3b-be96-a0f7b01f7642,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
7a7a8e27-621f-4e3b-be96-a0f7b01f7642,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
7a7a8e27-621f-4e3b-be96-a0f7b01f7642,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
7a7a8e27-621f-4e3b-be96-a0f7b01f7642,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
7a7a8e27-621f-4e3b-be96-a0f7b01f7642,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
7a7a8e27-621f-4e3b-be96-a0f7b01f7642,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
7a7a8e27-621f-4e3b-be96-a0f7b01f7642,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
7a7a8e27-621f-4e3b-be96-a0f7b01f7642,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
7a7a8e27-621f-4e3b-be96-a0f7b01f7642,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
7a7a8e27-621f-4e3b-be96-a0f7b01f7642,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
7a7a8e27-621f-4e3b-be96-a0f7b01f7642,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
7a7a8e27-621f-4e3b-be96-a0f7b01f7642,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
516b545d-c192-4faa-ae28-361434116ad2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"As hypokalemia also inhibits Na+-K+ ATPase, Na+ accumulates inside the cell. This in turn leads to an accumulation of Ca++ because of a subsequent failure of the Na+-Ca++ exchanger. Extended presence of these two positive ions inside the myocyte prolongs the action potential and may manifest as an increased width and amplitude of the P-wave.",True,Hyper- and Hypokalemia,,,,
2944c3f1-92b0-4f52-9542-738a4ed289fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"As hypokalemia worsens, the problems with K+ conductance and repolarization increase, and the myocardium becomes susceptible to early after-depolarization (EAD) arrhythmias.",True,Hyper- and Hypokalemia,,,,
591bca12-9802-451e-b8f6-5e659b26fde7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
591bca12-9802-451e-b8f6-5e659b26fde7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
591bca12-9802-451e-b8f6-5e659b26fde7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
591bca12-9802-451e-b8f6-5e659b26fde7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
591bca12-9802-451e-b8f6-5e659b26fde7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
591bca12-9802-451e-b8f6-5e659b26fde7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
591bca12-9802-451e-b8f6-5e659b26fde7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
591bca12-9802-451e-b8f6-5e659b26fde7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
591bca12-9802-451e-b8f6-5e659b26fde7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
591bca12-9802-451e-b8f6-5e659b26fde7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
591bca12-9802-451e-b8f6-5e659b26fde7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
591bca12-9802-451e-b8f6-5e659b26fde7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
591bca12-9802-451e-b8f6-5e659b26fde7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
591bca12-9802-451e-b8f6-5e659b26fde7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
591bca12-9802-451e-b8f6-5e659b26fde7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
591bca12-9802-451e-b8f6-5e659b26fde7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
591bca12-9802-451e-b8f6-5e659b26fde7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a14b6853-11c7-4a1b-b3a6-2b510bd579a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
a14b6853-11c7-4a1b-b3a6-2b510bd579a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
a14b6853-11c7-4a1b-b3a6-2b510bd579a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
a14b6853-11c7-4a1b-b3a6-2b510bd579a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
a14b6853-11c7-4a1b-b3a6-2b510bd579a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
a14b6853-11c7-4a1b-b3a6-2b510bd579a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
a14b6853-11c7-4a1b-b3a6-2b510bd579a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
a14b6853-11c7-4a1b-b3a6-2b510bd579a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
a14b6853-11c7-4a1b-b3a6-2b510bd579a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
a14b6853-11c7-4a1b-b3a6-2b510bd579a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
a14b6853-11c7-4a1b-b3a6-2b510bd579a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
a14b6853-11c7-4a1b-b3a6-2b510bd579a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
a14b6853-11c7-4a1b-b3a6-2b510bd579a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
a14b6853-11c7-4a1b-b3a6-2b510bd579a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
a14b6853-11c7-4a1b-b3a6-2b510bd579a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
a14b6853-11c7-4a1b-b3a6-2b510bd579a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
a14b6853-11c7-4a1b-b3a6-2b510bd579a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
9447a1f7-fcec-4ada-9ab5-9baab5342034,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
9447a1f7-fcec-4ada-9ab5-9baab5342034,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
9447a1f7-fcec-4ada-9ab5-9baab5342034,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
9447a1f7-fcec-4ada-9ab5-9baab5342034,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
9447a1f7-fcec-4ada-9ab5-9baab5342034,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
9447a1f7-fcec-4ada-9ab5-9baab5342034,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
9447a1f7-fcec-4ada-9ab5-9baab5342034,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
9447a1f7-fcec-4ada-9ab5-9baab5342034,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
9447a1f7-fcec-4ada-9ab5-9baab5342034,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
9447a1f7-fcec-4ada-9ab5-9baab5342034,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
9447a1f7-fcec-4ada-9ab5-9baab5342034,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
9447a1f7-fcec-4ada-9ab5-9baab5342034,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
9447a1f7-fcec-4ada-9ab5-9baab5342034,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
9447a1f7-fcec-4ada-9ab5-9baab5342034,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
9447a1f7-fcec-4ada-9ab5-9baab5342034,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
9447a1f7-fcec-4ada-9ab5-9baab5342034,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
9447a1f7-fcec-4ada-9ab5-9baab5342034,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
66496271-4889-45e8-ae7b-5003ed70798a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
66496271-4889-45e8-ae7b-5003ed70798a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
66496271-4889-45e8-ae7b-5003ed70798a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
66496271-4889-45e8-ae7b-5003ed70798a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
66496271-4889-45e8-ae7b-5003ed70798a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
66496271-4889-45e8-ae7b-5003ed70798a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
66496271-4889-45e8-ae7b-5003ed70798a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
66496271-4889-45e8-ae7b-5003ed70798a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
66496271-4889-45e8-ae7b-5003ed70798a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
66496271-4889-45e8-ae7b-5003ed70798a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
66496271-4889-45e8-ae7b-5003ed70798a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
66496271-4889-45e8-ae7b-5003ed70798a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
66496271-4889-45e8-ae7b-5003ed70798a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
66496271-4889-45e8-ae7b-5003ed70798a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
66496271-4889-45e8-ae7b-5003ed70798a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
66496271-4889-45e8-ae7b-5003ed70798a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
66496271-4889-45e8-ae7b-5003ed70798a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
2974f6e4-5a96-4bbd-b554-a950f87a0614,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Table 1.17: Hypo- and hyperkalemia summary.,True,Hyper- and Hypokalemia,,,,
b81edf45-a37f-42cd-995a-5ed1b0bc18d7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"References, resources, and further reading",False,"References, resources, and further reading",,,,
12655efb-3f90-4b92-91bd-b6d60f6592a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,Text,False,Text,,,,
79ca5627-b478-47f4-bc3a-6db30a056fab,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Burns, Ed, and Robert Buttner. Hypercalcaemia. Lift in the Fast Lane, 2021. https://litfl.com/hypercalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
8a270007-4f50-4bed-b8ce-875b68031a7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Burns, Ed, and Robert Buttner. Hypocalcaemia. Life in the Fast Lane, 2021. https://litfl.com/hypocalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
b23fa539-7678-4e20-9850-69dd5f911c09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Buttner, Robert, and Ed Burns. Hyperkalaemia. Life in the Fast Lane. https://litfl.com/hyperkalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
ad6c3a63-92b4-4864-81b6-2e2053789448,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Buttner, Robert, and Ed Burns. Hypokalaemia. Life in the Fast Lane, 2021. https://litfl.com/hypokalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
28f78a22-81bd-4a8d-8f9d-45a59d8f9d4c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Chhabra, Lovely, Amandeep Goyal, and Michael D. Benham. Wolff Parkinson White Syndrome. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK554437/, CC BY 4.0.",True,Text,,,,
20d2abda-7f41-449d-8ebb-d19ff00c5e7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Custer, Adam M., Varun S. Yelamanchili, and Sarah L. Lappin. Multifocal Atrial Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459152/, CC BY 4.0.",True,Text,,,,
0c3994b0-2f46-49e6-a863-ce163228d573,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Farzam, Khashayar, and John R. Richards. Premature Ventricular Contraction. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532991/, CC BY 4.0.",True,Text,,,,
e3837fcc-f722-4495-be9a-98e5b7279244,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Foth, Christopher, Manesh Kumar Gangwani, and Heidi Alvey. Ventricular Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532954/, CC BY 4.0.",True,Text,,,,
7b16ced2-74a7-4347-9962-69a67a2d1ac9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Hafeez, Yamama, and Shamai A. Grossman. Sinus Bradycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK493201/, CC BY 4.0.",True,Text,,,,
d5b5fae2-3515-4766-90ca-25cf9f95613a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Harkness, Weston T., and Mary Hicks. Right Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK507872/, CC BY 4.0.",True,Text,,,,
ee68c68b-69be-47ab-8865-5dda4a1068ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Heaton, Joseph, and Srikanth Yandrapalli. Premature Atrial Contractions. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK559204/, CC BY 4.0.",True,Text,,,,
10d00462-1ceb-47ea-8bf2-f936e9c1cf49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Kashou, Anthony H., Amandeep Goyal, Tran Nguyen, and Lovely Chhabra. Atrioventricular Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459147/, CC BY 4.0.",True,Text,,,,
3b74871b-baab-46fc-8acc-4fac479cdce6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,“Learn the Heart.” Healio. https://www.healio.com/cardiology/learn-the-heart.,True,Text,,,,
a005c6d6-5edf-42bd-960e-e4543155afaa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Ludhwani, Dipesh, Amandeep Goyal, and Mandar Jagtap. Ventricular Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK537120/, CC BY 4.0.",True,Text,,,,
ed2e9cba-b63d-4b0c-bb2c-a5ca8629456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Nesheiwat, Zeid, Amandeep Goyal, and Mandar Jagtap. Atrial Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK526072/, CC BY 4.0.",True,Text,,,,
bd7c3fea-2c42-4b6c-bddc-6a9d685741d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Pipilas, Daniel C., Bruce A. Koplan, and Leonard S. Lilly. “The Electrocardiogram.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 4. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
ee9925e6-4648-49db-b004-1dbb9de25950,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Rodriguez Ziccardi, Mary, Amandeep Goyal, and Christopher V. Maani. Atrial Flutter. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK540985/, CC BY 4.0.",True,Text,,,,
90a944c3-d43a-4c10-8f83-92812936897e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-9,"Scherbak, Dmitriy, and Gregory J. Hicks. Left Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK482167/, CC BY 4.0.",True,Text,,,,
a29b3668-9090-41fe-96ef-f254a8f61491,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,USMLE,False,USMLE,,,,
539b3da0-ea2a-4aa2-874c-ce311721dc0d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
539b3da0-ea2a-4aa2-874c-ce311721dc0d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
539b3da0-ea2a-4aa2-874c-ce311721dc0d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
539b3da0-ea2a-4aa2-874c-ce311721dc0d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
539b3da0-ea2a-4aa2-874c-ce311721dc0d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
539b3da0-ea2a-4aa2-874c-ce311721dc0d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
539b3da0-ea2a-4aa2-874c-ce311721dc0d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
539b3da0-ea2a-4aa2-874c-ce311721dc0d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
539b3da0-ea2a-4aa2-874c-ce311721dc0d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
539b3da0-ea2a-4aa2-874c-ce311721dc0d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
539b3da0-ea2a-4aa2-874c-ce311721dc0d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
539b3da0-ea2a-4aa2-874c-ce311721dc0d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
539b3da0-ea2a-4aa2-874c-ce311721dc0d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
539b3da0-ea2a-4aa2-874c-ce311721dc0d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
539b3da0-ea2a-4aa2-874c-ce311721dc0d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
539b3da0-ea2a-4aa2-874c-ce311721dc0d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
539b3da0-ea2a-4aa2-874c-ce311721dc0d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
2d11733c-0591-4c32-8721-6f88ce7afdbc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,10q22,False,10q22,,,,
5a4890ee-f1ff-4f34-8d71-60dab4c0a006,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,q24,False,q24,,,,
cd71daf7-e78a-4d88-911c-70c3894421d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,fibrillatory,False,fibrillatory,,,,
d18e3fdf-b4af-4020-b88f-5ffb7a5fc58c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d18e3fdf-b4af-4020-b88f-5ffb7a5fc58c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d18e3fdf-b4af-4020-b88f-5ffb7a5fc58c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d18e3fdf-b4af-4020-b88f-5ffb7a5fc58c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d18e3fdf-b4af-4020-b88f-5ffb7a5fc58c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d18e3fdf-b4af-4020-b88f-5ffb7a5fc58c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d18e3fdf-b4af-4020-b88f-5ffb7a5fc58c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d18e3fdf-b4af-4020-b88f-5ffb7a5fc58c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d18e3fdf-b4af-4020-b88f-5ffb7a5fc58c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d18e3fdf-b4af-4020-b88f-5ffb7a5fc58c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d18e3fdf-b4af-4020-b88f-5ffb7a5fc58c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d18e3fdf-b4af-4020-b88f-5ffb7a5fc58c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d18e3fdf-b4af-4020-b88f-5ffb7a5fc58c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d18e3fdf-b4af-4020-b88f-5ffb7a5fc58c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d18e3fdf-b4af-4020-b88f-5ffb7a5fc58c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d18e3fdf-b4af-4020-b88f-5ffb7a5fc58c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d18e3fdf-b4af-4020-b88f-5ffb7a5fc58c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
cf179528-0c37-4469-93c6-d30a3b7d1f26,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Table 1.1: Atrial fibrillation summary.,True,fibrillatory,,,,
44affd8d-89cd-4c0f-9856-3726411e4fcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Atrial Flutter,False,Atrial Flutter,,,,
75ca7be6-bb05-4792-b98d-0db3d4cd327d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
75ca7be6-bb05-4792-b98d-0db3d4cd327d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
75ca7be6-bb05-4792-b98d-0db3d4cd327d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
75ca7be6-bb05-4792-b98d-0db3d4cd327d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
75ca7be6-bb05-4792-b98d-0db3d4cd327d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
75ca7be6-bb05-4792-b98d-0db3d4cd327d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
75ca7be6-bb05-4792-b98d-0db3d4cd327d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
75ca7be6-bb05-4792-b98d-0db3d4cd327d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
75ca7be6-bb05-4792-b98d-0db3d4cd327d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
75ca7be6-bb05-4792-b98d-0db3d4cd327d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
75ca7be6-bb05-4792-b98d-0db3d4cd327d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
75ca7be6-bb05-4792-b98d-0db3d4cd327d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
75ca7be6-bb05-4792-b98d-0db3d4cd327d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
75ca7be6-bb05-4792-b98d-0db3d4cd327d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
75ca7be6-bb05-4792-b98d-0db3d4cd327d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
75ca7be6-bb05-4792-b98d-0db3d4cd327d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
75ca7be6-bb05-4792-b98d-0db3d4cd327d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
99a23a0f-1c43-4431-b65c-de9bc789e36b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,macroreentrant,False,macroreentrant,,,,
423a5fda-8dc0-4e2a-92c4-766aa38f4759,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,cavotricuspid,False,cavotricuspid,,,,
fa6110a9-4547-4ba0-82f3-fffa143f3bad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"As with atrial fibrillation, the AV node’s refractory period prevents most of the P-waves from progressing to the ventricle, but commonly the AV conduction will be 2-to-1, so with an atrial rate of 300 bpm the ventricular rate will be 150 bpm. Parasympathetic stimulation or changes in AV node refractoriness can modify how many P-waves pass into the ventricle, but the the resultant rhythm is “regularly irregular.” When the heart rate is elevated, then distinguishing flutter from fibrillation becomes challenging and slowing ventricular rate pharmaceutically (adenosine) helps the flutter waves reemerge for a definitive diagnosis to be made.",True,cavotricuspid,,,,
fa1f3203-5943-4405-a156-54200c908785,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Table 1.2: Atrial flutter summary.,True,cavotricuspid,,,,
72524e19-a283-4234-a8e7-a691b11906e3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Multifocal Atrial Tachycardia,False,Multifocal Atrial Tachycardia,,,,
8d558bb2-80bc-46cb-9957-64544bc96423,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
8d558bb2-80bc-46cb-9957-64544bc96423,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
8d558bb2-80bc-46cb-9957-64544bc96423,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
8d558bb2-80bc-46cb-9957-64544bc96423,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
8d558bb2-80bc-46cb-9957-64544bc96423,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
8d558bb2-80bc-46cb-9957-64544bc96423,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
8d558bb2-80bc-46cb-9957-64544bc96423,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
8d558bb2-80bc-46cb-9957-64544bc96423,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
8d558bb2-80bc-46cb-9957-64544bc96423,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
8d558bb2-80bc-46cb-9957-64544bc96423,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
8d558bb2-80bc-46cb-9957-64544bc96423,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
8d558bb2-80bc-46cb-9957-64544bc96423,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
8d558bb2-80bc-46cb-9957-64544bc96423,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
8d558bb2-80bc-46cb-9957-64544bc96423,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
8d558bb2-80bc-46cb-9957-64544bc96423,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
8d558bb2-80bc-46cb-9957-64544bc96423,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
8d558bb2-80bc-46cb-9957-64544bc96423,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
44d651e1-b265-4d4e-a901-278023c79893,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"MAT frequently occurs in the setting of severe lung disease and, more specifically, during an exacerbation of lung disease. This rhythm is benign, and once the underlying lung disease is treated, it should resolve.",True,Multifocal Atrial Tachycardia,,,,
754a5f8f-fcc7-4cea-8c9d-b41141cee5ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Table 1.3: MAT summary.,True,Multifocal Atrial Tachycardia,,,,
f921dbdc-58a1-460d-999f-72ffaa33796c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Premature Atrial Contraction,False,Premature Atrial Contraction,,,,
31518638-204d-4b76-b6b8-931e6b785527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A premature atrial contraction (PAC) is generated by a depolarization instigated outside of the SA node. This produces an extra P-wave, and consequently a shortening from previous P-P intervals is seen. The aberrant P-wave also has a different morphology from a sinus P-wave because of its different anatomical origin.",True,Premature Atrial Contraction,,,,
f48cf1dd-01d1-43f7-a1ab-55f1cb0ca70a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
f48cf1dd-01d1-43f7-a1ab-55f1cb0ca70a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
f48cf1dd-01d1-43f7-a1ab-55f1cb0ca70a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
f48cf1dd-01d1-43f7-a1ab-55f1cb0ca70a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
f48cf1dd-01d1-43f7-a1ab-55f1cb0ca70a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
f48cf1dd-01d1-43f7-a1ab-55f1cb0ca70a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
f48cf1dd-01d1-43f7-a1ab-55f1cb0ca70a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
f48cf1dd-01d1-43f7-a1ab-55f1cb0ca70a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
f48cf1dd-01d1-43f7-a1ab-55f1cb0ca70a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
f48cf1dd-01d1-43f7-a1ab-55f1cb0ca70a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
f48cf1dd-01d1-43f7-a1ab-55f1cb0ca70a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
f48cf1dd-01d1-43f7-a1ab-55f1cb0ca70a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
f48cf1dd-01d1-43f7-a1ab-55f1cb0ca70a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
f48cf1dd-01d1-43f7-a1ab-55f1cb0ca70a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
f48cf1dd-01d1-43f7-a1ab-55f1cb0ca70a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
f48cf1dd-01d1-43f7-a1ab-55f1cb0ca70a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
f48cf1dd-01d1-43f7-a1ab-55f1cb0ca70a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
b0e3dbe1-fd89-4d45-a6a3-8e93f0dc2c3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"If a PAC occurs when the AV node has not yet recovered from its refractory period, the PAC will fail to conduct to the ventricles; meaning the PAC will not be followed by a QRS complex or the ectopic P-R interval will be prolonged. The ECG will show a premature, ectopic P-wave and then no QRS complex afterward. When this occurs along with bigeminy, the ECG can appear as if there is sinus bradycardia.",True,Premature Atrial Contraction,,,,
2a3c05d0-7b0f-4659-8c15-8d8b719d42b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Table 1.4: PAC summary.,True,Premature Atrial Contraction,,,,
f826ee55-a2be-4bcc-af9e-1e71031f0a86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Sinus Bradycardia,False,Sinus Bradycardia,,,,
e7ca9f08-223e-4dcf-9150-9ed88f7f4180,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Sinus bradycardia denotes a sinus rhythm below 60 bpm. Otherwise the ECG waveform is normal on an ECG with an upright P-wave in lead II preceding every QRS complex. There are many intrinsic causes associated with the heart itself, as well as extrinsic causes, some of which are listed table 1.5. Sinus bradycardia is usually asymptomatic as rates of 40–50 bpm can maintain hemodynamic stability. Rates below this can produce symptoms of fatigue, dizziness, and dyspnea on exertion.",True,Sinus Bradycardia,,,,
4be863ab-e9b7-4bbf-98e7-54f1f59c143d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Table 1.5: Intrinsic and extrinsic causes associated with the heart.,True,Sinus Bradycardia,,,,
f1bcaeea-f7f8-4768-b762-c1d44036542f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Table 1.6: Sinus bradycardia summary.,True,Sinus Bradycardia,,,,
6b437cc0-2e1e-4670-a9f0-aa1384686ee0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Premature Ventricular Contractions,False,Premature Ventricular Contractions,,,,
98d1fe0e-9144-4a9c-8789-a8359e8ccf41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
98d1fe0e-9144-4a9c-8789-a8359e8ccf41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
98d1fe0e-9144-4a9c-8789-a8359e8ccf41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
98d1fe0e-9144-4a9c-8789-a8359e8ccf41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
98d1fe0e-9144-4a9c-8789-a8359e8ccf41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
98d1fe0e-9144-4a9c-8789-a8359e8ccf41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
98d1fe0e-9144-4a9c-8789-a8359e8ccf41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
98d1fe0e-9144-4a9c-8789-a8359e8ccf41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
98d1fe0e-9144-4a9c-8789-a8359e8ccf41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
98d1fe0e-9144-4a9c-8789-a8359e8ccf41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
98d1fe0e-9144-4a9c-8789-a8359e8ccf41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
98d1fe0e-9144-4a9c-8789-a8359e8ccf41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
98d1fe0e-9144-4a9c-8789-a8359e8ccf41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
98d1fe0e-9144-4a9c-8789-a8359e8ccf41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
98d1fe0e-9144-4a9c-8789-a8359e8ccf41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
98d1fe0e-9144-4a9c-8789-a8359e8ccf41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
98d1fe0e-9144-4a9c-8789-a8359e8ccf41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3fb89168-b1cd-4494-87d2-580e0d43c12a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Table 1.7: PVC summary.,True,Premature Ventricular Contractions,,,,
af32e720-9891-409b-80ab-3266ddafc61d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Ventricular Tachycardia,False,Ventricular Tachycardia,,,,
52a5929e-7df6-481d-b010-58cad61c7e84,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Ventricular tachycardia (VT) is caused by reentry currents being established in the ventricular myocardium or groups of ventricular myocytes that have aberrant electrical behavior. As such, VT is usually caused by underlying cardiac disease.",True,Ventricular Tachycardia,,,,
898ada89-4a7b-45af-94e1-86fd74853854,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Like a PVC, the aberrant depolarizations do not follow the normal conduction pathways so are wide (>120 msecs), but unlike a PVC, VT involves a ventricular rate >100 bpm. With disorganized contractility and reduced filling time, VT can lead to hemodynamic instability and severe hypotension—hence it is life threatening.",True,Ventricular Tachycardia,,,,
b9786e18-f264-49b6-93c4-4d97adcf082e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The QRS morphology in VT is highly variable between patients and depends on where the arrhythmia originates. Consequently there are several ways to classify VT based on duration, symptoms, QRS morphology, rate, and origin.",True,Ventricular Tachycardia,,,,
31189c82-27ff-4139-8547-87fc96fea4be,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Sustained VT is any VT that lasts for more than 30 seconds or is symptomatic. Nonsustained VT lasts for less than 30 seconds and is asymptomatic.,True,Ventricular Tachycardia,,,,
d69481da-7397-4338-99a7-c2be83de2077,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d69481da-7397-4338-99a7-c2be83de2077,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d69481da-7397-4338-99a7-c2be83de2077,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d69481da-7397-4338-99a7-c2be83de2077,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d69481da-7397-4338-99a7-c2be83de2077,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d69481da-7397-4338-99a7-c2be83de2077,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d69481da-7397-4338-99a7-c2be83de2077,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d69481da-7397-4338-99a7-c2be83de2077,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d69481da-7397-4338-99a7-c2be83de2077,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d69481da-7397-4338-99a7-c2be83de2077,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d69481da-7397-4338-99a7-c2be83de2077,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d69481da-7397-4338-99a7-c2be83de2077,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d69481da-7397-4338-99a7-c2be83de2077,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d69481da-7397-4338-99a7-c2be83de2077,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d69481da-7397-4338-99a7-c2be83de2077,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d69481da-7397-4338-99a7-c2be83de2077,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d69481da-7397-4338-99a7-c2be83de2077,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
a5ab1db2-fa39-4bb3-ae83-1e88448ca87b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a5ab1db2-fa39-4bb3-ae83-1e88448ca87b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a5ab1db2-fa39-4bb3-ae83-1e88448ca87b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a5ab1db2-fa39-4bb3-ae83-1e88448ca87b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a5ab1db2-fa39-4bb3-ae83-1e88448ca87b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a5ab1db2-fa39-4bb3-ae83-1e88448ca87b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a5ab1db2-fa39-4bb3-ae83-1e88448ca87b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a5ab1db2-fa39-4bb3-ae83-1e88448ca87b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a5ab1db2-fa39-4bb3-ae83-1e88448ca87b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a5ab1db2-fa39-4bb3-ae83-1e88448ca87b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a5ab1db2-fa39-4bb3-ae83-1e88448ca87b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a5ab1db2-fa39-4bb3-ae83-1e88448ca87b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a5ab1db2-fa39-4bb3-ae83-1e88448ca87b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a5ab1db2-fa39-4bb3-ae83-1e88448ca87b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a5ab1db2-fa39-4bb3-ae83-1e88448ca87b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a5ab1db2-fa39-4bb3-ae83-1e88448ca87b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a5ab1db2-fa39-4bb3-ae83-1e88448ca87b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
cacd2d7f-932a-497c-9445-7092949b1038,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Torsades de pointes is associated with a prolonged QT interval (>600 msecs) that helps distinguish it from other forms of polymorphous VT. The longer QT interval can be caused by ionic abnormalities that reduce the repolarizing current of Phase 3 of the cardiac action potential. This makes the myocardium susceptible to early after-depolarizations—the trigger for torsades de pointes. These after-depolarizations do not happen uniformly across the myocardium and are more common in endocardial tissue where the repolarization currents are slower. So torsades de pointes arises from the after-depolarizations causing reentry currents in neighboring tissue.,True,Ventricular Tachycardia,,,,
831305d7-9724-4cee-8466-c165790f89cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Both common garden variety VTs and torsades de pointes can progress to ventricular fibrillation.,True,Ventricular Tachycardia,,,,
ecddee2f-84eb-4cd3-a64f-2acb07074427,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Table 1.8: VT summary.,True,Ventricular Tachycardia,,,,
9d9beabf-f116-48bb-b27e-1ea0b7cb954d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Ventricular Fibrillation,False,Ventricular Fibrillation,,,,
930a03d2-a7ed-4bcb-8a92-f7ccef63dcf6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Ventricular fibrillation (VF) occurs when the ventricular rate exceeds 400 bpm. The disorganized and uncoordinated contraction of the myocardium causes cardiac output to fall to catastrophic levels. Rates of survival for out-of-hospital VF are low.,True,Ventricular Fibrillation,,,,
aaf07662-15d1-4650-8cb8-f4b1bff438da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
aaf07662-15d1-4650-8cb8-f4b1bff438da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
aaf07662-15d1-4650-8cb8-f4b1bff438da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
aaf07662-15d1-4650-8cb8-f4b1bff438da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
aaf07662-15d1-4650-8cb8-f4b1bff438da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
aaf07662-15d1-4650-8cb8-f4b1bff438da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
aaf07662-15d1-4650-8cb8-f4b1bff438da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
aaf07662-15d1-4650-8cb8-f4b1bff438da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
aaf07662-15d1-4650-8cb8-f4b1bff438da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
aaf07662-15d1-4650-8cb8-f4b1bff438da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
aaf07662-15d1-4650-8cb8-f4b1bff438da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
aaf07662-15d1-4650-8cb8-f4b1bff438da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
aaf07662-15d1-4650-8cb8-f4b1bff438da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
aaf07662-15d1-4650-8cb8-f4b1bff438da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
aaf07662-15d1-4650-8cb8-f4b1bff438da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
aaf07662-15d1-4650-8cb8-f4b1bff438da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
aaf07662-15d1-4650-8cb8-f4b1bff438da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
9c47ebb4-4bf6-416b-8508-f607d07e19f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Table 1.9: VF summary.,True,Ventricular Fibrillation,,,,
a3500c41-9d2d-475a-9599-f2222f57bfd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,First-Degree Atrioventricular Block,False,First-Degree Atrioventricular Block,,,,
1fab0cce-4a78-4615-871b-9c257924950b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1fab0cce-4a78-4615-871b-9c257924950b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1fab0cce-4a78-4615-871b-9c257924950b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1fab0cce-4a78-4615-871b-9c257924950b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1fab0cce-4a78-4615-871b-9c257924950b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1fab0cce-4a78-4615-871b-9c257924950b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1fab0cce-4a78-4615-871b-9c257924950b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1fab0cce-4a78-4615-871b-9c257924950b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1fab0cce-4a78-4615-871b-9c257924950b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1fab0cce-4a78-4615-871b-9c257924950b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1fab0cce-4a78-4615-871b-9c257924950b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1fab0cce-4a78-4615-871b-9c257924950b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1fab0cce-4a78-4615-871b-9c257924950b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1fab0cce-4a78-4615-871b-9c257924950b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1fab0cce-4a78-4615-871b-9c257924950b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1fab0cce-4a78-4615-871b-9c257924950b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
1fab0cce-4a78-4615-871b-9c257924950b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8497ab37-384d-4d10-b05c-bfde6edfe9a0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8497ab37-384d-4d10-b05c-bfde6edfe9a0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8497ab37-384d-4d10-b05c-bfde6edfe9a0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8497ab37-384d-4d10-b05c-bfde6edfe9a0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8497ab37-384d-4d10-b05c-bfde6edfe9a0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8497ab37-384d-4d10-b05c-bfde6edfe9a0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8497ab37-384d-4d10-b05c-bfde6edfe9a0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8497ab37-384d-4d10-b05c-bfde6edfe9a0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8497ab37-384d-4d10-b05c-bfde6edfe9a0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8497ab37-384d-4d10-b05c-bfde6edfe9a0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8497ab37-384d-4d10-b05c-bfde6edfe9a0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8497ab37-384d-4d10-b05c-bfde6edfe9a0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8497ab37-384d-4d10-b05c-bfde6edfe9a0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8497ab37-384d-4d10-b05c-bfde6edfe9a0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8497ab37-384d-4d10-b05c-bfde6edfe9a0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8497ab37-384d-4d10-b05c-bfde6edfe9a0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8497ab37-384d-4d10-b05c-bfde6edfe9a0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ce0c9d99-64ab-47a9-a406-84266f420d76,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Table 1.10: First-degree block summary.,True,First-Degree Atrioventricular Block,,,,
cf1980b0-6901-48ea-ad97-aee29885acf4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Second-Degree Atrioventricular Block,False,Second-Degree Atrioventricular Block,,,,
3914d3b6-afa2-4781-8c78-2e554370fe64,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A second-degree atrioventricular block also has changes in P-R interval, but it starts to show failure of the P-wave to propagate a QRS complex every time (i.e., intermittently the depolarization fails to reach the ventricles). The pattern of missed ventricular depolarizations, or blocked P-waves, is often very regular and described as a ratio of P-waves to QRS complex. The way in which the P-R interval changes in relation to the blocked P-waves produces subclassifications of second-degree blocks, Mobitz I and II.",True,Second-Degree Atrioventricular Block,,,,
ff08658a-f880-47c4-a435-285da249bed9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
ff08658a-f880-47c4-a435-285da249bed9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
ff08658a-f880-47c4-a435-285da249bed9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
ff08658a-f880-47c4-a435-285da249bed9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
ff08658a-f880-47c4-a435-285da249bed9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
ff08658a-f880-47c4-a435-285da249bed9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
ff08658a-f880-47c4-a435-285da249bed9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
ff08658a-f880-47c4-a435-285da249bed9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
ff08658a-f880-47c4-a435-285da249bed9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
ff08658a-f880-47c4-a435-285da249bed9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
ff08658a-f880-47c4-a435-285da249bed9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
ff08658a-f880-47c4-a435-285da249bed9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
ff08658a-f880-47c4-a435-285da249bed9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
ff08658a-f880-47c4-a435-285da249bed9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
ff08658a-f880-47c4-a435-285da249bed9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
ff08658a-f880-47c4-a435-285da249bed9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
ff08658a-f880-47c4-a435-285da249bed9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
cfbf26d1-7544-4775-8c90-6b0a8a46c124,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
cfbf26d1-7544-4775-8c90-6b0a8a46c124,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
cfbf26d1-7544-4775-8c90-6b0a8a46c124,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
cfbf26d1-7544-4775-8c90-6b0a8a46c124,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
cfbf26d1-7544-4775-8c90-6b0a8a46c124,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
cfbf26d1-7544-4775-8c90-6b0a8a46c124,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
cfbf26d1-7544-4775-8c90-6b0a8a46c124,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
cfbf26d1-7544-4775-8c90-6b0a8a46c124,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
cfbf26d1-7544-4775-8c90-6b0a8a46c124,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
cfbf26d1-7544-4775-8c90-6b0a8a46c124,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
cfbf26d1-7544-4775-8c90-6b0a8a46c124,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
cfbf26d1-7544-4775-8c90-6b0a8a46c124,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
cfbf26d1-7544-4775-8c90-6b0a8a46c124,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
cfbf26d1-7544-4775-8c90-6b0a8a46c124,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
cfbf26d1-7544-4775-8c90-6b0a8a46c124,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
cfbf26d1-7544-4775-8c90-6b0a8a46c124,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
cfbf26d1-7544-4775-8c90-6b0a8a46c124,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
fce89b13-638c-4ac5-909d-0ae6345694c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Table 1.11: Second-degree block summary.,True,Second-Degree Atrioventricular Block,,,,
b619d8ce-c844-470c-9795-7f029925c6dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Third-Degree Atrioventricular Block,False,Third-Degree Atrioventricular Block,,,,
d0e62168-6f27-470a-a7c5-d7c7333342c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
d0e62168-6f27-470a-a7c5-d7c7333342c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
d0e62168-6f27-470a-a7c5-d7c7333342c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
d0e62168-6f27-470a-a7c5-d7c7333342c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
d0e62168-6f27-470a-a7c5-d7c7333342c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
d0e62168-6f27-470a-a7c5-d7c7333342c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
d0e62168-6f27-470a-a7c5-d7c7333342c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
d0e62168-6f27-470a-a7c5-d7c7333342c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
d0e62168-6f27-470a-a7c5-d7c7333342c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
d0e62168-6f27-470a-a7c5-d7c7333342c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
d0e62168-6f27-470a-a7c5-d7c7333342c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
d0e62168-6f27-470a-a7c5-d7c7333342c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
d0e62168-6f27-470a-a7c5-d7c7333342c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
d0e62168-6f27-470a-a7c5-d7c7333342c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
d0e62168-6f27-470a-a7c5-d7c7333342c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
d0e62168-6f27-470a-a7c5-d7c7333342c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
d0e62168-6f27-470a-a7c5-d7c7333342c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
dad1df55-8613-4071-a34b-a21fc9c09303,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Table 1.12: Third-degree block summary.,True,Third-Degree Atrioventricular Block,,,,
3533b0ad-9f34-499b-9d80-739f289e379e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Left Bundle Branch Block,False,Left Bundle Branch Block,,,,
d46651f5-6865-4091-861a-0bab73c4b5c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"A left bundle branch block (LBBB) is generated when the conductivity of the His-Purkinje system in the left ventricle is compromised, either through damage or disease. The ECG changes, and criteria for LBBB relate to these changes in conductivity and the left-side location.",True,Left Bundle Branch Block,,,,
a5b8dacc-1d21-4da4-8317-2eb47f18529d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a5b8dacc-1d21-4da4-8317-2eb47f18529d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a5b8dacc-1d21-4da4-8317-2eb47f18529d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a5b8dacc-1d21-4da4-8317-2eb47f18529d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a5b8dacc-1d21-4da4-8317-2eb47f18529d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a5b8dacc-1d21-4da4-8317-2eb47f18529d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a5b8dacc-1d21-4da4-8317-2eb47f18529d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a5b8dacc-1d21-4da4-8317-2eb47f18529d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a5b8dacc-1d21-4da4-8317-2eb47f18529d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a5b8dacc-1d21-4da4-8317-2eb47f18529d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a5b8dacc-1d21-4da4-8317-2eb47f18529d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a5b8dacc-1d21-4da4-8317-2eb47f18529d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a5b8dacc-1d21-4da4-8317-2eb47f18529d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a5b8dacc-1d21-4da4-8317-2eb47f18529d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a5b8dacc-1d21-4da4-8317-2eb47f18529d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a5b8dacc-1d21-4da4-8317-2eb47f18529d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
a5b8dacc-1d21-4da4-8317-2eb47f18529d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
def70313-ee0a-4ad8-bbb1-40f11dbec308,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The lateral leads (I, V5, and V6) normally show a downward deflecting Q-wave as normal septal deflection initially occurs left-to-right (i.e., away from the lateral leads). In LBBB the change in direction to right-to-left, plus the longer duration, eliminates the Q-wave from the lateral leads, and Q-waves will be small in aVL.",True,Left Bundle Branch Block,,,,
6778ae8b-625d-44fe-89ca-3be85e7b645e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
6778ae8b-625d-44fe-89ca-3be85e7b645e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
6778ae8b-625d-44fe-89ca-3be85e7b645e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
6778ae8b-625d-44fe-89ca-3be85e7b645e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
6778ae8b-625d-44fe-89ca-3be85e7b645e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
6778ae8b-625d-44fe-89ca-3be85e7b645e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
6778ae8b-625d-44fe-89ca-3be85e7b645e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
6778ae8b-625d-44fe-89ca-3be85e7b645e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
6778ae8b-625d-44fe-89ca-3be85e7b645e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
6778ae8b-625d-44fe-89ca-3be85e7b645e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
6778ae8b-625d-44fe-89ca-3be85e7b645e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
6778ae8b-625d-44fe-89ca-3be85e7b645e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
6778ae8b-625d-44fe-89ca-3be85e7b645e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
6778ae8b-625d-44fe-89ca-3be85e7b645e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
6778ae8b-625d-44fe-89ca-3be85e7b645e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
6778ae8b-625d-44fe-89ca-3be85e7b645e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
6778ae8b-625d-44fe-89ca-3be85e7b645e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
78e5b20e-cb49-49ad-a333-bb262b589bcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
78e5b20e-cb49-49ad-a333-bb262b589bcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
78e5b20e-cb49-49ad-a333-bb262b589bcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
78e5b20e-cb49-49ad-a333-bb262b589bcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
78e5b20e-cb49-49ad-a333-bb262b589bcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
78e5b20e-cb49-49ad-a333-bb262b589bcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
78e5b20e-cb49-49ad-a333-bb262b589bcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
78e5b20e-cb49-49ad-a333-bb262b589bcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
78e5b20e-cb49-49ad-a333-bb262b589bcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
78e5b20e-cb49-49ad-a333-bb262b589bcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
78e5b20e-cb49-49ad-a333-bb262b589bcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
78e5b20e-cb49-49ad-a333-bb262b589bcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
78e5b20e-cb49-49ad-a333-bb262b589bcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
78e5b20e-cb49-49ad-a333-bb262b589bcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
78e5b20e-cb49-49ad-a333-bb262b589bcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
78e5b20e-cb49-49ad-a333-bb262b589bcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
78e5b20e-cb49-49ad-a333-bb262b589bcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
0ab8e631-6827-4491-b4eb-c8231e3600e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Table 1.13: LBBB summary.,True,Left Bundle Branch Block,,,,
e2caba27-16de-47ab-8b98-22902551e0bf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Right Bundle Branch Block,False,Right Bundle Branch Block,,,,
533066e4-f58e-41a2-b276-fb85b9051e3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The causes and manifestations of a right bundle branch block (RBBB) bear some similarities to those described for LBBB, but of course this time its depolarization of the right ventricle is delayed. Causes of RBBB include ischemic heart disease again as well as other myocardial diseases, but pulmonary issues such as pulmonary embolism and cor pulmonale can be added to the list.",True,Right Bundle Branch Block,,,,
c7bceb7f-c40c-417e-9c89-4be14a34451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
c7bceb7f-c40c-417e-9c89-4be14a34451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
c7bceb7f-c40c-417e-9c89-4be14a34451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
c7bceb7f-c40c-417e-9c89-4be14a34451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
c7bceb7f-c40c-417e-9c89-4be14a34451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
c7bceb7f-c40c-417e-9c89-4be14a34451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
c7bceb7f-c40c-417e-9c89-4be14a34451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
c7bceb7f-c40c-417e-9c89-4be14a34451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
c7bceb7f-c40c-417e-9c89-4be14a34451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
c7bceb7f-c40c-417e-9c89-4be14a34451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
c7bceb7f-c40c-417e-9c89-4be14a34451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
c7bceb7f-c40c-417e-9c89-4be14a34451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
c7bceb7f-c40c-417e-9c89-4be14a34451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
c7bceb7f-c40c-417e-9c89-4be14a34451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
c7bceb7f-c40c-417e-9c89-4be14a34451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
c7bceb7f-c40c-417e-9c89-4be14a34451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
c7bceb7f-c40c-417e-9c89-4be14a34451c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
c79eecad-5cfb-4879-83e8-4a4cea2ad9bf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Table 1.14: RBBB summary.,True,Right Bundle Branch Block,,,,
01eb7f34-10fd-4a55-addf-c1dcc4f66301,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Wolff-Parkinson-White Syndrome,False,Wolff-Parkinson-White Syndrome,,,,
ac64eab8-ebf9-4b98-b963-a3ce8723ebc3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Normally the only electrical connection between the atria and the ventricles is the AV node. Otherwise the fibrous skeleton of the heart electrically insulates the atria from the ventricles. In Wolff-Parkinson-White (WPW) syndrome, that insulation is incomplete, and an “accessory pathway” connects the electrical system of the atria directly to the ventricles. If you think of the AV node as a bridge over the fibrous wall with regulated access, the accessory pathway is like a pathological tunnel under it with no regulation.",True,Wolff-Parkinson-White Syndrome,,,,
fd5d790d-680d-4b82-9346-f4411ecc15cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
fd5d790d-680d-4b82-9346-f4411ecc15cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
fd5d790d-680d-4b82-9346-f4411ecc15cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
fd5d790d-680d-4b82-9346-f4411ecc15cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
fd5d790d-680d-4b82-9346-f4411ecc15cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
fd5d790d-680d-4b82-9346-f4411ecc15cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
fd5d790d-680d-4b82-9346-f4411ecc15cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
fd5d790d-680d-4b82-9346-f4411ecc15cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
fd5d790d-680d-4b82-9346-f4411ecc15cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
fd5d790d-680d-4b82-9346-f4411ecc15cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
fd5d790d-680d-4b82-9346-f4411ecc15cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
fd5d790d-680d-4b82-9346-f4411ecc15cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
fd5d790d-680d-4b82-9346-f4411ecc15cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
fd5d790d-680d-4b82-9346-f4411ecc15cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
fd5d790d-680d-4b82-9346-f4411ecc15cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
fd5d790d-680d-4b82-9346-f4411ecc15cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
fd5d790d-680d-4b82-9346-f4411ecc15cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
718d0b08-42ba-4530-a623-13291e5a9be4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"WPW syndrome is often asymptomatic, and patients do not require immediate treatment. However, if atrial fibrillation occurs in a WPW patient, the accessory pathway can allow the atrial fibrillation waves through to the ventricle (with no AV nodal refractory period to prevent them). Consequently a high ventricular rate is seen, and the risk of ventricular fibrillation being established means immediate clinical attention is required.",True,Wolff-Parkinson-White Syndrome,,,,
a94cd893-7a8e-44ab-b845-6bd77e33c0a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Hyper- and Hypocalcemia,False,Hyper- and Hypocalcemia,,,,
3d933bed-43a2-4909-a008-8c408e2fc0ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3d933bed-43a2-4909-a008-8c408e2fc0ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3d933bed-43a2-4909-a008-8c408e2fc0ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3d933bed-43a2-4909-a008-8c408e2fc0ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3d933bed-43a2-4909-a008-8c408e2fc0ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3d933bed-43a2-4909-a008-8c408e2fc0ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3d933bed-43a2-4909-a008-8c408e2fc0ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3d933bed-43a2-4909-a008-8c408e2fc0ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3d933bed-43a2-4909-a008-8c408e2fc0ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3d933bed-43a2-4909-a008-8c408e2fc0ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3d933bed-43a2-4909-a008-8c408e2fc0ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3d933bed-43a2-4909-a008-8c408e2fc0ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3d933bed-43a2-4909-a008-8c408e2fc0ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3d933bed-43a2-4909-a008-8c408e2fc0ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3d933bed-43a2-4909-a008-8c408e2fc0ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3d933bed-43a2-4909-a008-8c408e2fc0ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3d933bed-43a2-4909-a008-8c408e2fc0ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
eaaec274-e6a0-4a9c-9244-62205125d8f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
eaaec274-e6a0-4a9c-9244-62205125d8f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
eaaec274-e6a0-4a9c-9244-62205125d8f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
eaaec274-e6a0-4a9c-9244-62205125d8f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
eaaec274-e6a0-4a9c-9244-62205125d8f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
eaaec274-e6a0-4a9c-9244-62205125d8f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
eaaec274-e6a0-4a9c-9244-62205125d8f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
eaaec274-e6a0-4a9c-9244-62205125d8f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
eaaec274-e6a0-4a9c-9244-62205125d8f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
eaaec274-e6a0-4a9c-9244-62205125d8f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
eaaec274-e6a0-4a9c-9244-62205125d8f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
eaaec274-e6a0-4a9c-9244-62205125d8f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
eaaec274-e6a0-4a9c-9244-62205125d8f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
eaaec274-e6a0-4a9c-9244-62205125d8f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
eaaec274-e6a0-4a9c-9244-62205125d8f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
eaaec274-e6a0-4a9c-9244-62205125d8f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
eaaec274-e6a0-4a9c-9244-62205125d8f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
e917caaa-739d-4135-9348-ea75d1c5c003,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Table 1.16: Hyper- and hypocalcemia summary.,True,Hyper- and Hypocalcemia,,,,
b6b6ecae-db14-4882-b4d2-a6092e3e1bff,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Hyper- and Hypokalemia,False,Hyper- and Hypokalemia,,,,
5300e361-1f6b-4939-a522-9fac461e7a06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"The pathophysiology is not as simple as changes in extracellular K+ changing the electrochemical gradient for K+. Because of potassium’s role in maintaining the resting membrane potential, shifts in extracellular potassium can also influence the activity of Na+ and Ca++ channels.",True,Hyper- and Hypokalemia,,,,
2de641d5-e55f-4304-ac96-b3c975773b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2de641d5-e55f-4304-ac96-b3c975773b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2de641d5-e55f-4304-ac96-b3c975773b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2de641d5-e55f-4304-ac96-b3c975773b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2de641d5-e55f-4304-ac96-b3c975773b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2de641d5-e55f-4304-ac96-b3c975773b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2de641d5-e55f-4304-ac96-b3c975773b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2de641d5-e55f-4304-ac96-b3c975773b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2de641d5-e55f-4304-ac96-b3c975773b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2de641d5-e55f-4304-ac96-b3c975773b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2de641d5-e55f-4304-ac96-b3c975773b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2de641d5-e55f-4304-ac96-b3c975773b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2de641d5-e55f-4304-ac96-b3c975773b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2de641d5-e55f-4304-ac96-b3c975773b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2de641d5-e55f-4304-ac96-b3c975773b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2de641d5-e55f-4304-ac96-b3c975773b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
2de641d5-e55f-4304-ac96-b3c975773b8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
262d6826-a03c-4781-8efb-e9a58555b9c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"As hypokalemia also inhibits Na+-K+ ATPase, Na+ accumulates inside the cell. This in turn leads to an accumulation of Ca++ because of a subsequent failure of the Na+-Ca++ exchanger. Extended presence of these two positive ions inside the myocyte prolongs the action potential and may manifest as an increased width and amplitude of the P-wave.",True,Hyper- and Hypokalemia,,,,
3b5b3b81-8de0-4ad8-962d-7c38a02625e3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"As hypokalemia worsens, the problems with K+ conductance and repolarization increase, and the myocardium becomes susceptible to early after-depolarization (EAD) arrhythmias.",True,Hyper- and Hypokalemia,,,,
d7e4d129-642d-4a03-8c2f-11d5e2ac2e44,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
d7e4d129-642d-4a03-8c2f-11d5e2ac2e44,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
d7e4d129-642d-4a03-8c2f-11d5e2ac2e44,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
d7e4d129-642d-4a03-8c2f-11d5e2ac2e44,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
d7e4d129-642d-4a03-8c2f-11d5e2ac2e44,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
d7e4d129-642d-4a03-8c2f-11d5e2ac2e44,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
d7e4d129-642d-4a03-8c2f-11d5e2ac2e44,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
d7e4d129-642d-4a03-8c2f-11d5e2ac2e44,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
d7e4d129-642d-4a03-8c2f-11d5e2ac2e44,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
d7e4d129-642d-4a03-8c2f-11d5e2ac2e44,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
d7e4d129-642d-4a03-8c2f-11d5e2ac2e44,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
d7e4d129-642d-4a03-8c2f-11d5e2ac2e44,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
d7e4d129-642d-4a03-8c2f-11d5e2ac2e44,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
d7e4d129-642d-4a03-8c2f-11d5e2ac2e44,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
d7e4d129-642d-4a03-8c2f-11d5e2ac2e44,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
d7e4d129-642d-4a03-8c2f-11d5e2ac2e44,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
d7e4d129-642d-4a03-8c2f-11d5e2ac2e44,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
20c2cb1a-879f-4c17-bf8f-cf67277bd49d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
20c2cb1a-879f-4c17-bf8f-cf67277bd49d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
20c2cb1a-879f-4c17-bf8f-cf67277bd49d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
20c2cb1a-879f-4c17-bf8f-cf67277bd49d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
20c2cb1a-879f-4c17-bf8f-cf67277bd49d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
20c2cb1a-879f-4c17-bf8f-cf67277bd49d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
20c2cb1a-879f-4c17-bf8f-cf67277bd49d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
20c2cb1a-879f-4c17-bf8f-cf67277bd49d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
20c2cb1a-879f-4c17-bf8f-cf67277bd49d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
20c2cb1a-879f-4c17-bf8f-cf67277bd49d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
20c2cb1a-879f-4c17-bf8f-cf67277bd49d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
20c2cb1a-879f-4c17-bf8f-cf67277bd49d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
20c2cb1a-879f-4c17-bf8f-cf67277bd49d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
20c2cb1a-879f-4c17-bf8f-cf67277bd49d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
20c2cb1a-879f-4c17-bf8f-cf67277bd49d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
20c2cb1a-879f-4c17-bf8f-cf67277bd49d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
20c2cb1a-879f-4c17-bf8f-cf67277bd49d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
b8a5a013-72f6-4864-9217-b73825c45c79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8a5a013-72f6-4864-9217-b73825c45c79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8a5a013-72f6-4864-9217-b73825c45c79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8a5a013-72f6-4864-9217-b73825c45c79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8a5a013-72f6-4864-9217-b73825c45c79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8a5a013-72f6-4864-9217-b73825c45c79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8a5a013-72f6-4864-9217-b73825c45c79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8a5a013-72f6-4864-9217-b73825c45c79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8a5a013-72f6-4864-9217-b73825c45c79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8a5a013-72f6-4864-9217-b73825c45c79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8a5a013-72f6-4864-9217-b73825c45c79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8a5a013-72f6-4864-9217-b73825c45c79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8a5a013-72f6-4864-9217-b73825c45c79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8a5a013-72f6-4864-9217-b73825c45c79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8a5a013-72f6-4864-9217-b73825c45c79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8a5a013-72f6-4864-9217-b73825c45c79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
b8a5a013-72f6-4864-9217-b73825c45c79,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
bacc4ca6-6d18-4424-a41b-49908d6d4d38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
bacc4ca6-6d18-4424-a41b-49908d6d4d38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
bacc4ca6-6d18-4424-a41b-49908d6d4d38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
bacc4ca6-6d18-4424-a41b-49908d6d4d38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
bacc4ca6-6d18-4424-a41b-49908d6d4d38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
bacc4ca6-6d18-4424-a41b-49908d6d4d38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
bacc4ca6-6d18-4424-a41b-49908d6d4d38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
bacc4ca6-6d18-4424-a41b-49908d6d4d38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
bacc4ca6-6d18-4424-a41b-49908d6d4d38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
bacc4ca6-6d18-4424-a41b-49908d6d4d38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
bacc4ca6-6d18-4424-a41b-49908d6d4d38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
bacc4ca6-6d18-4424-a41b-49908d6d4d38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
bacc4ca6-6d18-4424-a41b-49908d6d4d38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
bacc4ca6-6d18-4424-a41b-49908d6d4d38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
bacc4ca6-6d18-4424-a41b-49908d6d4d38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
bacc4ca6-6d18-4424-a41b-49908d6d4d38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
bacc4ca6-6d18-4424-a41b-49908d6d4d38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fcee266d-789f-4360-b0eb-96b3b4c9c479,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Table 1.17: Hypo- and hyperkalemia summary.,True,Hyper- and Hypokalemia,,,,
49ce9af5-9403-483e-9cba-635bac861639,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"References, resources, and further reading",False,"References, resources, and further reading",,,,
4fbb1d2e-50ab-4588-9aae-bf8cf13f445f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,Text,False,Text,,,,
b264ef45-7727-4706-ab9b-14264ba077e3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Burns, Ed, and Robert Buttner. Hypercalcaemia. Lift in the Fast Lane, 2021. https://litfl.com/hypercalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
a9b465b4-7ca6-4bbc-a0dc-75d50d5c6902,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Burns, Ed, and Robert Buttner. Hypocalcaemia. Life in the Fast Lane, 2021. https://litfl.com/hypocalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
d94d9423-2532-446c-9fec-58f36599f297,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Buttner, Robert, and Ed Burns. Hyperkalaemia. Life in the Fast Lane. https://litfl.com/hyperkalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
ef25ebfe-da9b-42f6-bab2-f1bb1b37b637,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Buttner, Robert, and Ed Burns. Hypokalaemia. Life in the Fast Lane, 2021. https://litfl.com/hypokalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
84565931-e2e5-4094-b555-e3fc7dfad0b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Chhabra, Lovely, Amandeep Goyal, and Michael D. Benham. Wolff Parkinson White Syndrome. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK554437/, CC BY 4.0.",True,Text,,,,
8017c9c2-3c50-4fcb-a170-43e51cd12c2e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Custer, Adam M., Varun S. Yelamanchili, and Sarah L. Lappin. Multifocal Atrial Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459152/, CC BY 4.0.",True,Text,,,,
5e79102b-b74d-4398-ab19-04d6ecc47e9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Farzam, Khashayar, and John R. Richards. Premature Ventricular Contraction. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532991/, CC BY 4.0.",True,Text,,,,
6b5bf999-45b8-40e1-8f10-863b609a4cff,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Foth, Christopher, Manesh Kumar Gangwani, and Heidi Alvey. Ventricular Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532954/, CC BY 4.0.",True,Text,,,,
cc06fce0-e858-44af-86ae-f8c639c0f660,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Hafeez, Yamama, and Shamai A. Grossman. Sinus Bradycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK493201/, CC BY 4.0.",True,Text,,,,
55e5c3d6-c602-414b-a0e6-4470d2caa226,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Harkness, Weston T., and Mary Hicks. Right Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK507872/, CC BY 4.0.",True,Text,,,,
135b13d9-4894-4ff1-8d41-674d83cfdcb9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Heaton, Joseph, and Srikanth Yandrapalli. Premature Atrial Contractions. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK559204/, CC BY 4.0.",True,Text,,,,
6578f441-76b6-4cf6-93b3-0f753f772d50,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Kashou, Anthony H., Amandeep Goyal, Tran Nguyen, and Lovely Chhabra. Atrioventricular Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459147/, CC BY 4.0.",True,Text,,,,
0e54bf92-383a-413d-8792-e07e8e614b9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,“Learn the Heart.” Healio. https://www.healio.com/cardiology/learn-the-heart.,True,Text,,,,
cb22a790-8f81-4839-82e9-76c3f2fe7c6f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Ludhwani, Dipesh, Amandeep Goyal, and Mandar Jagtap. Ventricular Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK537120/, CC BY 4.0.",True,Text,,,,
3035624d-7074-4f80-a906-3a137ed9485a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Nesheiwat, Zeid, Amandeep Goyal, and Mandar Jagtap. Atrial Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK526072/, CC BY 4.0.",True,Text,,,,
15cb2715-da62-4716-a044-9ee1b1e82cc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Pipilas, Daniel C., Bruce A. Koplan, and Leonard S. Lilly. “The Electrocardiogram.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 4. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
ee5e2b6b-e84b-4bcf-a7c9-54061f2bcaa5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Rodriguez Ziccardi, Mary, Amandeep Goyal, and Christopher V. Maani. Atrial Flutter. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK540985/, CC BY 4.0.",True,Text,,,,
fcebed34-3116-40fa-9bce-6dfa74e76b9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-8,"Scherbak, Dmitriy, and Gregory J. Hicks. Left Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK482167/, CC BY 4.0.",True,Text,,,,
b8ce077e-290c-4452-9363-50050dd696b8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,USMLE,False,USMLE,,,,
43d4d1c9-cbfc-40ab-be75-b82d0b65199e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
43d4d1c9-cbfc-40ab-be75-b82d0b65199e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
43d4d1c9-cbfc-40ab-be75-b82d0b65199e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
43d4d1c9-cbfc-40ab-be75-b82d0b65199e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
43d4d1c9-cbfc-40ab-be75-b82d0b65199e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
43d4d1c9-cbfc-40ab-be75-b82d0b65199e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
43d4d1c9-cbfc-40ab-be75-b82d0b65199e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
43d4d1c9-cbfc-40ab-be75-b82d0b65199e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
43d4d1c9-cbfc-40ab-be75-b82d0b65199e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
43d4d1c9-cbfc-40ab-be75-b82d0b65199e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
43d4d1c9-cbfc-40ab-be75-b82d0b65199e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
43d4d1c9-cbfc-40ab-be75-b82d0b65199e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
43d4d1c9-cbfc-40ab-be75-b82d0b65199e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
43d4d1c9-cbfc-40ab-be75-b82d0b65199e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
43d4d1c9-cbfc-40ab-be75-b82d0b65199e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
43d4d1c9-cbfc-40ab-be75-b82d0b65199e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
43d4d1c9-cbfc-40ab-be75-b82d0b65199e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
dd200c3f-01e1-40b8-b178-ed0558871bc2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,10q22,False,10q22,,,,
59fc9148-98ea-40a6-92d7-c53c9e2abc47,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,q24,False,q24,,,,
fb3757ed-9a30-4232-8ec1-b0da13e586bf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,fibrillatory,False,fibrillatory,,,,
3dbc9217-d3c6-4967-83b9-d5cc164fae05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3dbc9217-d3c6-4967-83b9-d5cc164fae05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3dbc9217-d3c6-4967-83b9-d5cc164fae05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3dbc9217-d3c6-4967-83b9-d5cc164fae05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3dbc9217-d3c6-4967-83b9-d5cc164fae05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3dbc9217-d3c6-4967-83b9-d5cc164fae05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3dbc9217-d3c6-4967-83b9-d5cc164fae05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3dbc9217-d3c6-4967-83b9-d5cc164fae05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3dbc9217-d3c6-4967-83b9-d5cc164fae05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3dbc9217-d3c6-4967-83b9-d5cc164fae05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3dbc9217-d3c6-4967-83b9-d5cc164fae05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3dbc9217-d3c6-4967-83b9-d5cc164fae05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3dbc9217-d3c6-4967-83b9-d5cc164fae05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3dbc9217-d3c6-4967-83b9-d5cc164fae05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3dbc9217-d3c6-4967-83b9-d5cc164fae05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3dbc9217-d3c6-4967-83b9-d5cc164fae05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3dbc9217-d3c6-4967-83b9-d5cc164fae05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
0edabb85-7b0d-4ec9-a27e-de852548f14b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Table 1.1: Atrial fibrillation summary.,True,fibrillatory,,,,
4c99cea8-5639-4bb5-b463-ab89772eb57e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Atrial Flutter,False,Atrial Flutter,,,,
bea4912d-0efa-41bc-815d-62d59c45e237,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bea4912d-0efa-41bc-815d-62d59c45e237,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bea4912d-0efa-41bc-815d-62d59c45e237,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bea4912d-0efa-41bc-815d-62d59c45e237,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bea4912d-0efa-41bc-815d-62d59c45e237,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bea4912d-0efa-41bc-815d-62d59c45e237,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bea4912d-0efa-41bc-815d-62d59c45e237,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bea4912d-0efa-41bc-815d-62d59c45e237,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bea4912d-0efa-41bc-815d-62d59c45e237,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bea4912d-0efa-41bc-815d-62d59c45e237,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bea4912d-0efa-41bc-815d-62d59c45e237,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bea4912d-0efa-41bc-815d-62d59c45e237,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bea4912d-0efa-41bc-815d-62d59c45e237,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bea4912d-0efa-41bc-815d-62d59c45e237,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bea4912d-0efa-41bc-815d-62d59c45e237,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bea4912d-0efa-41bc-815d-62d59c45e237,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
bea4912d-0efa-41bc-815d-62d59c45e237,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
b5b65fad-3420-4471-a078-9398f9037d98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,macroreentrant,False,macroreentrant,,,,
5d5e96ee-ba74-4e15-b099-c2dcc40090fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,cavotricuspid,False,cavotricuspid,,,,
96105f22-2e43-4b89-b077-d7b190c8d6af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"As with atrial fibrillation, the AV node’s refractory period prevents most of the P-waves from progressing to the ventricle, but commonly the AV conduction will be 2-to-1, so with an atrial rate of 300 bpm the ventricular rate will be 150 bpm. Parasympathetic stimulation or changes in AV node refractoriness can modify how many P-waves pass into the ventricle, but the the resultant rhythm is “regularly irregular.” When the heart rate is elevated, then distinguishing flutter from fibrillation becomes challenging and slowing ventricular rate pharmaceutically (adenosine) helps the flutter waves reemerge for a definitive diagnosis to be made.",True,cavotricuspid,,,,
8a082f48-d5df-4d21-8dc7-c31e6dce4aab,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Table 1.2: Atrial flutter summary.,True,cavotricuspid,,,,
a2c6038a-8cb0-4f46-aac0-86ea8414bafd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Multifocal Atrial Tachycardia,False,Multifocal Atrial Tachycardia,,,,
35ecaf36-6bb5-40cb-896f-7b4be82405d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
35ecaf36-6bb5-40cb-896f-7b4be82405d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
35ecaf36-6bb5-40cb-896f-7b4be82405d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
35ecaf36-6bb5-40cb-896f-7b4be82405d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
35ecaf36-6bb5-40cb-896f-7b4be82405d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
35ecaf36-6bb5-40cb-896f-7b4be82405d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
35ecaf36-6bb5-40cb-896f-7b4be82405d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
35ecaf36-6bb5-40cb-896f-7b4be82405d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
35ecaf36-6bb5-40cb-896f-7b4be82405d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
35ecaf36-6bb5-40cb-896f-7b4be82405d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
35ecaf36-6bb5-40cb-896f-7b4be82405d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
35ecaf36-6bb5-40cb-896f-7b4be82405d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
35ecaf36-6bb5-40cb-896f-7b4be82405d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
35ecaf36-6bb5-40cb-896f-7b4be82405d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
35ecaf36-6bb5-40cb-896f-7b4be82405d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
35ecaf36-6bb5-40cb-896f-7b4be82405d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
35ecaf36-6bb5-40cb-896f-7b4be82405d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
89fe4a88-f52f-4ff8-a167-ab5891e7a3b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"MAT frequently occurs in the setting of severe lung disease and, more specifically, during an exacerbation of lung disease. This rhythm is benign, and once the underlying lung disease is treated, it should resolve.",True,Multifocal Atrial Tachycardia,,,,
d8243c68-6f8b-4dd0-aa6b-f8193fc3df6c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Table 1.3: MAT summary.,True,Multifocal Atrial Tachycardia,,,,
ead4601c-6d4a-4125-a367-2411d2f3d71c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Premature Atrial Contraction,False,Premature Atrial Contraction,,,,
4bdcf6e4-dd35-461a-a499-6f1fed5cae27,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A premature atrial contraction (PAC) is generated by a depolarization instigated outside of the SA node. This produces an extra P-wave, and consequently a shortening from previous P-P intervals is seen. The aberrant P-wave also has a different morphology from a sinus P-wave because of its different anatomical origin.",True,Premature Atrial Contraction,,,,
5e2176f0-b4f5-46d4-b54e-578f4ae5c517,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
5e2176f0-b4f5-46d4-b54e-578f4ae5c517,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
5e2176f0-b4f5-46d4-b54e-578f4ae5c517,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
5e2176f0-b4f5-46d4-b54e-578f4ae5c517,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
5e2176f0-b4f5-46d4-b54e-578f4ae5c517,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
5e2176f0-b4f5-46d4-b54e-578f4ae5c517,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
5e2176f0-b4f5-46d4-b54e-578f4ae5c517,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
5e2176f0-b4f5-46d4-b54e-578f4ae5c517,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
5e2176f0-b4f5-46d4-b54e-578f4ae5c517,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
5e2176f0-b4f5-46d4-b54e-578f4ae5c517,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
5e2176f0-b4f5-46d4-b54e-578f4ae5c517,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
5e2176f0-b4f5-46d4-b54e-578f4ae5c517,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
5e2176f0-b4f5-46d4-b54e-578f4ae5c517,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
5e2176f0-b4f5-46d4-b54e-578f4ae5c517,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
5e2176f0-b4f5-46d4-b54e-578f4ae5c517,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
5e2176f0-b4f5-46d4-b54e-578f4ae5c517,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
5e2176f0-b4f5-46d4-b54e-578f4ae5c517,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
42d5753d-7c05-4080-a8e9-68004187debe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"If a PAC occurs when the AV node has not yet recovered from its refractory period, the PAC will fail to conduct to the ventricles; meaning the PAC will not be followed by a QRS complex or the ectopic P-R interval will be prolonged. The ECG will show a premature, ectopic P-wave and then no QRS complex afterward. When this occurs along with bigeminy, the ECG can appear as if there is sinus bradycardia.",True,Premature Atrial Contraction,,,,
42fccc7c-7492-4bd1-9695-2f9a1441a454,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Table 1.4: PAC summary.,True,Premature Atrial Contraction,,,,
96830bee-8dbb-4c08-9cc2-76428464a216,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Sinus Bradycardia,False,Sinus Bradycardia,,,,
3e05aced-8ec6-492f-a4d6-cc8b464d89fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Sinus bradycardia denotes a sinus rhythm below 60 bpm. Otherwise the ECG waveform is normal on an ECG with an upright P-wave in lead II preceding every QRS complex. There are many intrinsic causes associated with the heart itself, as well as extrinsic causes, some of which are listed table 1.5. Sinus bradycardia is usually asymptomatic as rates of 40–50 bpm can maintain hemodynamic stability. Rates below this can produce symptoms of fatigue, dizziness, and dyspnea on exertion.",True,Sinus Bradycardia,,,,
1840ef66-12dc-41b0-96df-6eab071d458f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Table 1.5: Intrinsic and extrinsic causes associated with the heart.,True,Sinus Bradycardia,,,,
f2fc0cd7-e6df-4dd2-ba20-ca3f8c18ba20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Table 1.6: Sinus bradycardia summary.,True,Sinus Bradycardia,,,,
1553d4e6-7ae7-43ba-a793-17c85bf0e1af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Premature Ventricular Contractions,False,Premature Ventricular Contractions,,,,
180e9d8c-2a22-4465-944e-797248373c11,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
180e9d8c-2a22-4465-944e-797248373c11,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
180e9d8c-2a22-4465-944e-797248373c11,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
180e9d8c-2a22-4465-944e-797248373c11,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
180e9d8c-2a22-4465-944e-797248373c11,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
180e9d8c-2a22-4465-944e-797248373c11,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
180e9d8c-2a22-4465-944e-797248373c11,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
180e9d8c-2a22-4465-944e-797248373c11,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
180e9d8c-2a22-4465-944e-797248373c11,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
180e9d8c-2a22-4465-944e-797248373c11,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
180e9d8c-2a22-4465-944e-797248373c11,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
180e9d8c-2a22-4465-944e-797248373c11,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
180e9d8c-2a22-4465-944e-797248373c11,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
180e9d8c-2a22-4465-944e-797248373c11,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
180e9d8c-2a22-4465-944e-797248373c11,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
180e9d8c-2a22-4465-944e-797248373c11,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
180e9d8c-2a22-4465-944e-797248373c11,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
5907f7d8-0210-4be6-a7f9-7d6e1881932f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Table 1.7: PVC summary.,True,Premature Ventricular Contractions,,,,
2e8c1a46-1f9d-417a-9c26-74c821627483,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Ventricular Tachycardia,False,Ventricular Tachycardia,,,,
2d79c36e-90f4-4f39-9709-360cd85aba13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Ventricular tachycardia (VT) is caused by reentry currents being established in the ventricular myocardium or groups of ventricular myocytes that have aberrant electrical behavior. As such, VT is usually caused by underlying cardiac disease.",True,Ventricular Tachycardia,,,,
b3f25239-0cc9-4410-b3df-b343fc0d83eb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Like a PVC, the aberrant depolarizations do not follow the normal conduction pathways so are wide (>120 msecs), but unlike a PVC, VT involves a ventricular rate >100 bpm. With disorganized contractility and reduced filling time, VT can lead to hemodynamic instability and severe hypotension—hence it is life threatening.",True,Ventricular Tachycardia,,,,
9ab2cd0f-c476-48b5-a138-7e1f1378b37c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The QRS morphology in VT is highly variable between patients and depends on where the arrhythmia originates. Consequently there are several ways to classify VT based on duration, symptoms, QRS morphology, rate, and origin.",True,Ventricular Tachycardia,,,,
cef39799-87f8-432d-af01-82e87b1efb60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Sustained VT is any VT that lasts for more than 30 seconds or is symptomatic. Nonsustained VT lasts for less than 30 seconds and is asymptomatic.,True,Ventricular Tachycardia,,,,
f2cf9469-2488-4105-a21b-4cbe833deb8f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f2cf9469-2488-4105-a21b-4cbe833deb8f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f2cf9469-2488-4105-a21b-4cbe833deb8f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f2cf9469-2488-4105-a21b-4cbe833deb8f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f2cf9469-2488-4105-a21b-4cbe833deb8f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f2cf9469-2488-4105-a21b-4cbe833deb8f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f2cf9469-2488-4105-a21b-4cbe833deb8f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f2cf9469-2488-4105-a21b-4cbe833deb8f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f2cf9469-2488-4105-a21b-4cbe833deb8f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f2cf9469-2488-4105-a21b-4cbe833deb8f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f2cf9469-2488-4105-a21b-4cbe833deb8f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f2cf9469-2488-4105-a21b-4cbe833deb8f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f2cf9469-2488-4105-a21b-4cbe833deb8f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f2cf9469-2488-4105-a21b-4cbe833deb8f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f2cf9469-2488-4105-a21b-4cbe833deb8f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f2cf9469-2488-4105-a21b-4cbe833deb8f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f2cf9469-2488-4105-a21b-4cbe833deb8f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
6dc9e90a-e80e-461f-b4d6-c596c19c8590,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
6dc9e90a-e80e-461f-b4d6-c596c19c8590,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
6dc9e90a-e80e-461f-b4d6-c596c19c8590,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
6dc9e90a-e80e-461f-b4d6-c596c19c8590,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
6dc9e90a-e80e-461f-b4d6-c596c19c8590,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
6dc9e90a-e80e-461f-b4d6-c596c19c8590,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
6dc9e90a-e80e-461f-b4d6-c596c19c8590,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
6dc9e90a-e80e-461f-b4d6-c596c19c8590,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
6dc9e90a-e80e-461f-b4d6-c596c19c8590,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
6dc9e90a-e80e-461f-b4d6-c596c19c8590,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
6dc9e90a-e80e-461f-b4d6-c596c19c8590,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
6dc9e90a-e80e-461f-b4d6-c596c19c8590,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
6dc9e90a-e80e-461f-b4d6-c596c19c8590,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
6dc9e90a-e80e-461f-b4d6-c596c19c8590,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
6dc9e90a-e80e-461f-b4d6-c596c19c8590,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
6dc9e90a-e80e-461f-b4d6-c596c19c8590,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
6dc9e90a-e80e-461f-b4d6-c596c19c8590,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
bdc2ef90-b87a-4867-966b-77895299882e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Torsades de pointes is associated with a prolonged QT interval (>600 msecs) that helps distinguish it from other forms of polymorphous VT. The longer QT interval can be caused by ionic abnormalities that reduce the repolarizing current of Phase 3 of the cardiac action potential. This makes the myocardium susceptible to early after-depolarizations—the trigger for torsades de pointes. These after-depolarizations do not happen uniformly across the myocardium and are more common in endocardial tissue where the repolarization currents are slower. So torsades de pointes arises from the after-depolarizations causing reentry currents in neighboring tissue.,True,Ventricular Tachycardia,,,,
d62b9491-da5d-4dc2-b44e-2d08cb5a923f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Both common garden variety VTs and torsades de pointes can progress to ventricular fibrillation.,True,Ventricular Tachycardia,,,,
a246e5c5-d446-4924-9838-5280e36403b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Table 1.8: VT summary.,True,Ventricular Tachycardia,,,,
61fad17f-e28c-4527-897a-1925a46f11b5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Ventricular Fibrillation,False,Ventricular Fibrillation,,,,
067b07ac-5ccf-4c3c-ab4a-3a0ca4b36415,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Ventricular fibrillation (VF) occurs when the ventricular rate exceeds 400 bpm. The disorganized and uncoordinated contraction of the myocardium causes cardiac output to fall to catastrophic levels. Rates of survival for out-of-hospital VF are low.,True,Ventricular Fibrillation,,,,
0e34534a-3814-4a1c-839e-be870f98f38f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0e34534a-3814-4a1c-839e-be870f98f38f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0e34534a-3814-4a1c-839e-be870f98f38f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0e34534a-3814-4a1c-839e-be870f98f38f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0e34534a-3814-4a1c-839e-be870f98f38f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0e34534a-3814-4a1c-839e-be870f98f38f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0e34534a-3814-4a1c-839e-be870f98f38f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0e34534a-3814-4a1c-839e-be870f98f38f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0e34534a-3814-4a1c-839e-be870f98f38f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0e34534a-3814-4a1c-839e-be870f98f38f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0e34534a-3814-4a1c-839e-be870f98f38f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0e34534a-3814-4a1c-839e-be870f98f38f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0e34534a-3814-4a1c-839e-be870f98f38f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0e34534a-3814-4a1c-839e-be870f98f38f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0e34534a-3814-4a1c-839e-be870f98f38f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0e34534a-3814-4a1c-839e-be870f98f38f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0e34534a-3814-4a1c-839e-be870f98f38f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
e5b8437c-c437-4b0a-8474-106b4d469eb5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Table 1.9: VF summary.,True,Ventricular Fibrillation,,,,
fd1666e9-9d32-45fa-a033-916b3b3efb3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,First-Degree Atrioventricular Block,False,First-Degree Atrioventricular Block,,,,
3530d913-7615-4b59-aa80-4c258cd99f3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3530d913-7615-4b59-aa80-4c258cd99f3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3530d913-7615-4b59-aa80-4c258cd99f3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3530d913-7615-4b59-aa80-4c258cd99f3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3530d913-7615-4b59-aa80-4c258cd99f3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3530d913-7615-4b59-aa80-4c258cd99f3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3530d913-7615-4b59-aa80-4c258cd99f3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3530d913-7615-4b59-aa80-4c258cd99f3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3530d913-7615-4b59-aa80-4c258cd99f3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3530d913-7615-4b59-aa80-4c258cd99f3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3530d913-7615-4b59-aa80-4c258cd99f3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3530d913-7615-4b59-aa80-4c258cd99f3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3530d913-7615-4b59-aa80-4c258cd99f3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3530d913-7615-4b59-aa80-4c258cd99f3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3530d913-7615-4b59-aa80-4c258cd99f3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3530d913-7615-4b59-aa80-4c258cd99f3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
3530d913-7615-4b59-aa80-4c258cd99f3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba01d724-c3aa-4a09-b190-a35f77b71316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba01d724-c3aa-4a09-b190-a35f77b71316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba01d724-c3aa-4a09-b190-a35f77b71316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba01d724-c3aa-4a09-b190-a35f77b71316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba01d724-c3aa-4a09-b190-a35f77b71316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba01d724-c3aa-4a09-b190-a35f77b71316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba01d724-c3aa-4a09-b190-a35f77b71316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba01d724-c3aa-4a09-b190-a35f77b71316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba01d724-c3aa-4a09-b190-a35f77b71316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba01d724-c3aa-4a09-b190-a35f77b71316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba01d724-c3aa-4a09-b190-a35f77b71316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba01d724-c3aa-4a09-b190-a35f77b71316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba01d724-c3aa-4a09-b190-a35f77b71316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba01d724-c3aa-4a09-b190-a35f77b71316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba01d724-c3aa-4a09-b190-a35f77b71316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba01d724-c3aa-4a09-b190-a35f77b71316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
ba01d724-c3aa-4a09-b190-a35f77b71316,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f0a13fab-257c-4821-911b-5070b2a9d6e0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Table 1.10: First-degree block summary.,True,First-Degree Atrioventricular Block,,,,
d7f1a540-283c-4976-833d-86ddf2ab6ff9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Second-Degree Atrioventricular Block,False,Second-Degree Atrioventricular Block,,,,
3cb22934-810b-470a-a0d4-1208101cf6aa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A second-degree atrioventricular block also has changes in P-R interval, but it starts to show failure of the P-wave to propagate a QRS complex every time (i.e., intermittently the depolarization fails to reach the ventricles). The pattern of missed ventricular depolarizations, or blocked P-waves, is often very regular and described as a ratio of P-waves to QRS complex. The way in which the P-R interval changes in relation to the blocked P-waves produces subclassifications of second-degree blocks, Mobitz I and II.",True,Second-Degree Atrioventricular Block,,,,
bfb3cce9-a155-4765-ad89-6b9c12cb1b65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
bfb3cce9-a155-4765-ad89-6b9c12cb1b65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
bfb3cce9-a155-4765-ad89-6b9c12cb1b65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
bfb3cce9-a155-4765-ad89-6b9c12cb1b65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
bfb3cce9-a155-4765-ad89-6b9c12cb1b65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
bfb3cce9-a155-4765-ad89-6b9c12cb1b65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
bfb3cce9-a155-4765-ad89-6b9c12cb1b65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
bfb3cce9-a155-4765-ad89-6b9c12cb1b65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
bfb3cce9-a155-4765-ad89-6b9c12cb1b65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
bfb3cce9-a155-4765-ad89-6b9c12cb1b65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
bfb3cce9-a155-4765-ad89-6b9c12cb1b65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
bfb3cce9-a155-4765-ad89-6b9c12cb1b65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
bfb3cce9-a155-4765-ad89-6b9c12cb1b65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
bfb3cce9-a155-4765-ad89-6b9c12cb1b65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
bfb3cce9-a155-4765-ad89-6b9c12cb1b65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
bfb3cce9-a155-4765-ad89-6b9c12cb1b65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
bfb3cce9-a155-4765-ad89-6b9c12cb1b65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
73a4280d-5d55-4200-b57e-e98225805762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
73a4280d-5d55-4200-b57e-e98225805762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
73a4280d-5d55-4200-b57e-e98225805762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
73a4280d-5d55-4200-b57e-e98225805762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
73a4280d-5d55-4200-b57e-e98225805762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
73a4280d-5d55-4200-b57e-e98225805762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
73a4280d-5d55-4200-b57e-e98225805762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
73a4280d-5d55-4200-b57e-e98225805762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
73a4280d-5d55-4200-b57e-e98225805762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
73a4280d-5d55-4200-b57e-e98225805762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
73a4280d-5d55-4200-b57e-e98225805762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
73a4280d-5d55-4200-b57e-e98225805762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
73a4280d-5d55-4200-b57e-e98225805762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
73a4280d-5d55-4200-b57e-e98225805762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
73a4280d-5d55-4200-b57e-e98225805762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
73a4280d-5d55-4200-b57e-e98225805762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
73a4280d-5d55-4200-b57e-e98225805762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
8250922a-4273-4103-aeb2-9db8f3c406a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Table 1.11: Second-degree block summary.,True,Second-Degree Atrioventricular Block,,,,
3e989494-4d18-44bd-961f-1273f80f001a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Third-Degree Atrioventricular Block,False,Third-Degree Atrioventricular Block,,,,
372c4497-e05a-405a-85bd-74543a2f54bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
372c4497-e05a-405a-85bd-74543a2f54bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
372c4497-e05a-405a-85bd-74543a2f54bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
372c4497-e05a-405a-85bd-74543a2f54bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
372c4497-e05a-405a-85bd-74543a2f54bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
372c4497-e05a-405a-85bd-74543a2f54bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
372c4497-e05a-405a-85bd-74543a2f54bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
372c4497-e05a-405a-85bd-74543a2f54bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
372c4497-e05a-405a-85bd-74543a2f54bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
372c4497-e05a-405a-85bd-74543a2f54bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
372c4497-e05a-405a-85bd-74543a2f54bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
372c4497-e05a-405a-85bd-74543a2f54bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
372c4497-e05a-405a-85bd-74543a2f54bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
372c4497-e05a-405a-85bd-74543a2f54bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
372c4497-e05a-405a-85bd-74543a2f54bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
372c4497-e05a-405a-85bd-74543a2f54bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
372c4497-e05a-405a-85bd-74543a2f54bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
e29a7475-40af-4f68-a924-b46b1c315de7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Table 1.12: Third-degree block summary.,True,Third-Degree Atrioventricular Block,,,,
b9d7601e-733e-451a-a123-4ba06c164bd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Left Bundle Branch Block,False,Left Bundle Branch Block,,,,
19d09611-a591-456d-b4aa-cadf203e5f6b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"A left bundle branch block (LBBB) is generated when the conductivity of the His-Purkinje system in the left ventricle is compromised, either through damage or disease. The ECG changes, and criteria for LBBB relate to these changes in conductivity and the left-side location.",True,Left Bundle Branch Block,,,,
95d13870-83b9-4669-a7d9-5370853d6762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
95d13870-83b9-4669-a7d9-5370853d6762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
95d13870-83b9-4669-a7d9-5370853d6762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
95d13870-83b9-4669-a7d9-5370853d6762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
95d13870-83b9-4669-a7d9-5370853d6762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
95d13870-83b9-4669-a7d9-5370853d6762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
95d13870-83b9-4669-a7d9-5370853d6762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
95d13870-83b9-4669-a7d9-5370853d6762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
95d13870-83b9-4669-a7d9-5370853d6762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
95d13870-83b9-4669-a7d9-5370853d6762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
95d13870-83b9-4669-a7d9-5370853d6762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
95d13870-83b9-4669-a7d9-5370853d6762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
95d13870-83b9-4669-a7d9-5370853d6762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
95d13870-83b9-4669-a7d9-5370853d6762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
95d13870-83b9-4669-a7d9-5370853d6762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
95d13870-83b9-4669-a7d9-5370853d6762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
95d13870-83b9-4669-a7d9-5370853d6762,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
1d5dd38a-b54f-42b9-a895-120ad452de3c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The lateral leads (I, V5, and V6) normally show a downward deflecting Q-wave as normal septal deflection initially occurs left-to-right (i.e., away from the lateral leads). In LBBB the change in direction to right-to-left, plus the longer duration, eliminates the Q-wave from the lateral leads, and Q-waves will be small in aVL.",True,Left Bundle Branch Block,,,,
f292e0af-34d1-415a-9e08-eb57eefa8616,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f292e0af-34d1-415a-9e08-eb57eefa8616,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f292e0af-34d1-415a-9e08-eb57eefa8616,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f292e0af-34d1-415a-9e08-eb57eefa8616,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f292e0af-34d1-415a-9e08-eb57eefa8616,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f292e0af-34d1-415a-9e08-eb57eefa8616,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f292e0af-34d1-415a-9e08-eb57eefa8616,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f292e0af-34d1-415a-9e08-eb57eefa8616,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f292e0af-34d1-415a-9e08-eb57eefa8616,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f292e0af-34d1-415a-9e08-eb57eefa8616,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f292e0af-34d1-415a-9e08-eb57eefa8616,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f292e0af-34d1-415a-9e08-eb57eefa8616,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f292e0af-34d1-415a-9e08-eb57eefa8616,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f292e0af-34d1-415a-9e08-eb57eefa8616,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f292e0af-34d1-415a-9e08-eb57eefa8616,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f292e0af-34d1-415a-9e08-eb57eefa8616,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
f292e0af-34d1-415a-9e08-eb57eefa8616,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
9bdf0ab8-fcd9-453d-ac71-9f84342d5e15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
9bdf0ab8-fcd9-453d-ac71-9f84342d5e15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
9bdf0ab8-fcd9-453d-ac71-9f84342d5e15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
9bdf0ab8-fcd9-453d-ac71-9f84342d5e15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
9bdf0ab8-fcd9-453d-ac71-9f84342d5e15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
9bdf0ab8-fcd9-453d-ac71-9f84342d5e15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
9bdf0ab8-fcd9-453d-ac71-9f84342d5e15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
9bdf0ab8-fcd9-453d-ac71-9f84342d5e15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
9bdf0ab8-fcd9-453d-ac71-9f84342d5e15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
9bdf0ab8-fcd9-453d-ac71-9f84342d5e15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
9bdf0ab8-fcd9-453d-ac71-9f84342d5e15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
9bdf0ab8-fcd9-453d-ac71-9f84342d5e15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
9bdf0ab8-fcd9-453d-ac71-9f84342d5e15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
9bdf0ab8-fcd9-453d-ac71-9f84342d5e15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
9bdf0ab8-fcd9-453d-ac71-9f84342d5e15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
9bdf0ab8-fcd9-453d-ac71-9f84342d5e15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
9bdf0ab8-fcd9-453d-ac71-9f84342d5e15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
fe5adf37-659e-42eb-a5f9-2e0fc2089592,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Table 1.13: LBBB summary.,True,Left Bundle Branch Block,,,,
a1d89b14-6c15-453b-a2f4-9c078b2b572e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Right Bundle Branch Block,False,Right Bundle Branch Block,,,,
bab76ac0-8c16-4222-af64-4d6d9a571c22,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The causes and manifestations of a right bundle branch block (RBBB) bear some similarities to those described for LBBB, but of course this time its depolarization of the right ventricle is delayed. Causes of RBBB include ischemic heart disease again as well as other myocardial diseases, but pulmonary issues such as pulmonary embolism and cor pulmonale can be added to the list.",True,Right Bundle Branch Block,,,,
e5aa009e-6bca-45d2-884a-7e80233b1afc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
e5aa009e-6bca-45d2-884a-7e80233b1afc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
e5aa009e-6bca-45d2-884a-7e80233b1afc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
e5aa009e-6bca-45d2-884a-7e80233b1afc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
e5aa009e-6bca-45d2-884a-7e80233b1afc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
e5aa009e-6bca-45d2-884a-7e80233b1afc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
e5aa009e-6bca-45d2-884a-7e80233b1afc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
e5aa009e-6bca-45d2-884a-7e80233b1afc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
e5aa009e-6bca-45d2-884a-7e80233b1afc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
e5aa009e-6bca-45d2-884a-7e80233b1afc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
e5aa009e-6bca-45d2-884a-7e80233b1afc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
e5aa009e-6bca-45d2-884a-7e80233b1afc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
e5aa009e-6bca-45d2-884a-7e80233b1afc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
e5aa009e-6bca-45d2-884a-7e80233b1afc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
e5aa009e-6bca-45d2-884a-7e80233b1afc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
e5aa009e-6bca-45d2-884a-7e80233b1afc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
e5aa009e-6bca-45d2-884a-7e80233b1afc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
9424a88e-c02d-41c7-819c-48106fd3cc68,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Table 1.14: RBBB summary.,True,Right Bundle Branch Block,,,,
81d453e2-ce3d-4d53-8443-6cd6a24a2226,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Wolff-Parkinson-White Syndrome,False,Wolff-Parkinson-White Syndrome,,,,
e9adc146-81b2-405c-8015-ddb2cc6624f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Normally the only electrical connection between the atria and the ventricles is the AV node. Otherwise the fibrous skeleton of the heart electrically insulates the atria from the ventricles. In Wolff-Parkinson-White (WPW) syndrome, that insulation is incomplete, and an “accessory pathway” connects the electrical system of the atria directly to the ventricles. If you think of the AV node as a bridge over the fibrous wall with regulated access, the accessory pathway is like a pathological tunnel under it with no regulation.",True,Wolff-Parkinson-White Syndrome,,,,
b7417502-9103-4ec1-99fc-8fd78f181c50,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
b7417502-9103-4ec1-99fc-8fd78f181c50,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
b7417502-9103-4ec1-99fc-8fd78f181c50,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
b7417502-9103-4ec1-99fc-8fd78f181c50,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
b7417502-9103-4ec1-99fc-8fd78f181c50,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
b7417502-9103-4ec1-99fc-8fd78f181c50,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
b7417502-9103-4ec1-99fc-8fd78f181c50,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
b7417502-9103-4ec1-99fc-8fd78f181c50,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
b7417502-9103-4ec1-99fc-8fd78f181c50,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
b7417502-9103-4ec1-99fc-8fd78f181c50,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
b7417502-9103-4ec1-99fc-8fd78f181c50,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
b7417502-9103-4ec1-99fc-8fd78f181c50,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
b7417502-9103-4ec1-99fc-8fd78f181c50,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
b7417502-9103-4ec1-99fc-8fd78f181c50,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
b7417502-9103-4ec1-99fc-8fd78f181c50,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
b7417502-9103-4ec1-99fc-8fd78f181c50,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
b7417502-9103-4ec1-99fc-8fd78f181c50,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
a11106de-665e-429c-8038-d03faf6bfc8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"WPW syndrome is often asymptomatic, and patients do not require immediate treatment. However, if atrial fibrillation occurs in a WPW patient, the accessory pathway can allow the atrial fibrillation waves through to the ventricle (with no AV nodal refractory period to prevent them). Consequently a high ventricular rate is seen, and the risk of ventricular fibrillation being established means immediate clinical attention is required.",True,Wolff-Parkinson-White Syndrome,,,,
2dd14f1f-12f8-4298-b9f9-02eb3f03c0f1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Hyper- and Hypocalcemia,False,Hyper- and Hypocalcemia,,,,
1e3b985a-8775-4384-9e47-90ff7e75fde8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
1e3b985a-8775-4384-9e47-90ff7e75fde8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
1e3b985a-8775-4384-9e47-90ff7e75fde8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
1e3b985a-8775-4384-9e47-90ff7e75fde8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
1e3b985a-8775-4384-9e47-90ff7e75fde8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
1e3b985a-8775-4384-9e47-90ff7e75fde8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
1e3b985a-8775-4384-9e47-90ff7e75fde8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
1e3b985a-8775-4384-9e47-90ff7e75fde8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
1e3b985a-8775-4384-9e47-90ff7e75fde8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
1e3b985a-8775-4384-9e47-90ff7e75fde8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
1e3b985a-8775-4384-9e47-90ff7e75fde8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
1e3b985a-8775-4384-9e47-90ff7e75fde8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
1e3b985a-8775-4384-9e47-90ff7e75fde8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
1e3b985a-8775-4384-9e47-90ff7e75fde8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
1e3b985a-8775-4384-9e47-90ff7e75fde8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
1e3b985a-8775-4384-9e47-90ff7e75fde8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
1e3b985a-8775-4384-9e47-90ff7e75fde8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
7b35b7c9-cbb6-4bbf-a5f3-0416bbd2e1bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
7b35b7c9-cbb6-4bbf-a5f3-0416bbd2e1bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
7b35b7c9-cbb6-4bbf-a5f3-0416bbd2e1bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
7b35b7c9-cbb6-4bbf-a5f3-0416bbd2e1bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
7b35b7c9-cbb6-4bbf-a5f3-0416bbd2e1bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
7b35b7c9-cbb6-4bbf-a5f3-0416bbd2e1bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
7b35b7c9-cbb6-4bbf-a5f3-0416bbd2e1bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
7b35b7c9-cbb6-4bbf-a5f3-0416bbd2e1bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
7b35b7c9-cbb6-4bbf-a5f3-0416bbd2e1bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
7b35b7c9-cbb6-4bbf-a5f3-0416bbd2e1bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
7b35b7c9-cbb6-4bbf-a5f3-0416bbd2e1bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
7b35b7c9-cbb6-4bbf-a5f3-0416bbd2e1bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
7b35b7c9-cbb6-4bbf-a5f3-0416bbd2e1bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
7b35b7c9-cbb6-4bbf-a5f3-0416bbd2e1bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
7b35b7c9-cbb6-4bbf-a5f3-0416bbd2e1bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
7b35b7c9-cbb6-4bbf-a5f3-0416bbd2e1bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
7b35b7c9-cbb6-4bbf-a5f3-0416bbd2e1bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
fb95b5fe-590e-4a13-8440-527d84ccab1a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Table 1.16: Hyper- and hypocalcemia summary.,True,Hyper- and Hypocalcemia,,,,
5e791ba0-5503-4d77-b61c-69c6f27f6b01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Hyper- and Hypokalemia,False,Hyper- and Hypokalemia,,,,
538d2fa6-230e-408b-b348-d78109e10afe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"The pathophysiology is not as simple as changes in extracellular K+ changing the electrochemical gradient for K+. Because of potassium’s role in maintaining the resting membrane potential, shifts in extracellular potassium can also influence the activity of Na+ and Ca++ channels.",True,Hyper- and Hypokalemia,,,,
70e4dc84-a559-494e-9d25-7576da9687da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
70e4dc84-a559-494e-9d25-7576da9687da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
70e4dc84-a559-494e-9d25-7576da9687da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
70e4dc84-a559-494e-9d25-7576da9687da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
70e4dc84-a559-494e-9d25-7576da9687da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
70e4dc84-a559-494e-9d25-7576da9687da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
70e4dc84-a559-494e-9d25-7576da9687da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
70e4dc84-a559-494e-9d25-7576da9687da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
70e4dc84-a559-494e-9d25-7576da9687da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
70e4dc84-a559-494e-9d25-7576da9687da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
70e4dc84-a559-494e-9d25-7576da9687da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
70e4dc84-a559-494e-9d25-7576da9687da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
70e4dc84-a559-494e-9d25-7576da9687da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
70e4dc84-a559-494e-9d25-7576da9687da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
70e4dc84-a559-494e-9d25-7576da9687da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
70e4dc84-a559-494e-9d25-7576da9687da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
70e4dc84-a559-494e-9d25-7576da9687da,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
cdeccc30-1b82-4c46-a38e-d4ef737036c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"As hypokalemia also inhibits Na+-K+ ATPase, Na+ accumulates inside the cell. This in turn leads to an accumulation of Ca++ because of a subsequent failure of the Na+-Ca++ exchanger. Extended presence of these two positive ions inside the myocyte prolongs the action potential and may manifest as an increased width and amplitude of the P-wave.",True,Hyper- and Hypokalemia,,,,
c5942f16-b90f-4445-b33e-fea9650bbbab,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"As hypokalemia worsens, the problems with K+ conductance and repolarization increase, and the myocardium becomes susceptible to early after-depolarization (EAD) arrhythmias.",True,Hyper- and Hypokalemia,,,,
3276ff1d-4531-482a-ad6f-dd3f403aec69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
3276ff1d-4531-482a-ad6f-dd3f403aec69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
3276ff1d-4531-482a-ad6f-dd3f403aec69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
3276ff1d-4531-482a-ad6f-dd3f403aec69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
3276ff1d-4531-482a-ad6f-dd3f403aec69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
3276ff1d-4531-482a-ad6f-dd3f403aec69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
3276ff1d-4531-482a-ad6f-dd3f403aec69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
3276ff1d-4531-482a-ad6f-dd3f403aec69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
3276ff1d-4531-482a-ad6f-dd3f403aec69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
3276ff1d-4531-482a-ad6f-dd3f403aec69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
3276ff1d-4531-482a-ad6f-dd3f403aec69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
3276ff1d-4531-482a-ad6f-dd3f403aec69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
3276ff1d-4531-482a-ad6f-dd3f403aec69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
3276ff1d-4531-482a-ad6f-dd3f403aec69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
3276ff1d-4531-482a-ad6f-dd3f403aec69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
3276ff1d-4531-482a-ad6f-dd3f403aec69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
3276ff1d-4531-482a-ad6f-dd3f403aec69,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
463f88ad-5fa5-4892-96a7-1edd3e45fe63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
463f88ad-5fa5-4892-96a7-1edd3e45fe63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
463f88ad-5fa5-4892-96a7-1edd3e45fe63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
463f88ad-5fa5-4892-96a7-1edd3e45fe63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
463f88ad-5fa5-4892-96a7-1edd3e45fe63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
463f88ad-5fa5-4892-96a7-1edd3e45fe63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
463f88ad-5fa5-4892-96a7-1edd3e45fe63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
463f88ad-5fa5-4892-96a7-1edd3e45fe63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
463f88ad-5fa5-4892-96a7-1edd3e45fe63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
463f88ad-5fa5-4892-96a7-1edd3e45fe63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
463f88ad-5fa5-4892-96a7-1edd3e45fe63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
463f88ad-5fa5-4892-96a7-1edd3e45fe63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
463f88ad-5fa5-4892-96a7-1edd3e45fe63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
463f88ad-5fa5-4892-96a7-1edd3e45fe63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
463f88ad-5fa5-4892-96a7-1edd3e45fe63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
463f88ad-5fa5-4892-96a7-1edd3e45fe63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
463f88ad-5fa5-4892-96a7-1edd3e45fe63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2cf1850c-68ad-4737-875b-eb888d83ac2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
2cf1850c-68ad-4737-875b-eb888d83ac2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
2cf1850c-68ad-4737-875b-eb888d83ac2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
2cf1850c-68ad-4737-875b-eb888d83ac2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
2cf1850c-68ad-4737-875b-eb888d83ac2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
2cf1850c-68ad-4737-875b-eb888d83ac2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
2cf1850c-68ad-4737-875b-eb888d83ac2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
2cf1850c-68ad-4737-875b-eb888d83ac2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
2cf1850c-68ad-4737-875b-eb888d83ac2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
2cf1850c-68ad-4737-875b-eb888d83ac2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
2cf1850c-68ad-4737-875b-eb888d83ac2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
2cf1850c-68ad-4737-875b-eb888d83ac2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
2cf1850c-68ad-4737-875b-eb888d83ac2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
2cf1850c-68ad-4737-875b-eb888d83ac2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
2cf1850c-68ad-4737-875b-eb888d83ac2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
2cf1850c-68ad-4737-875b-eb888d83ac2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
2cf1850c-68ad-4737-875b-eb888d83ac2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
f274182b-a036-42a2-8b87-3abcf611e1d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
f274182b-a036-42a2-8b87-3abcf611e1d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
f274182b-a036-42a2-8b87-3abcf611e1d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
f274182b-a036-42a2-8b87-3abcf611e1d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
f274182b-a036-42a2-8b87-3abcf611e1d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
f274182b-a036-42a2-8b87-3abcf611e1d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
f274182b-a036-42a2-8b87-3abcf611e1d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
f274182b-a036-42a2-8b87-3abcf611e1d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
f274182b-a036-42a2-8b87-3abcf611e1d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
f274182b-a036-42a2-8b87-3abcf611e1d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
f274182b-a036-42a2-8b87-3abcf611e1d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
f274182b-a036-42a2-8b87-3abcf611e1d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
f274182b-a036-42a2-8b87-3abcf611e1d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
f274182b-a036-42a2-8b87-3abcf611e1d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
f274182b-a036-42a2-8b87-3abcf611e1d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
f274182b-a036-42a2-8b87-3abcf611e1d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
f274182b-a036-42a2-8b87-3abcf611e1d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
869e979f-f682-4b7c-b545-af04fba0e064,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Table 1.17: Hypo- and hyperkalemia summary.,True,Hyper- and Hypokalemia,,,,
e90510c3-61e2-428c-828d-c657d63d0ccc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"References, resources, and further reading",False,"References, resources, and further reading",,,,
d8c2049c-c366-43de-8854-6280ea5adf03,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,Text,False,Text,,,,
c8dcd276-50d0-4e25-a6e5-253d726c82fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Burns, Ed, and Robert Buttner. Hypercalcaemia. Lift in the Fast Lane, 2021. https://litfl.com/hypercalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
c1a60c20-6c0e-48ee-8e19-e52adbddfb87,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Burns, Ed, and Robert Buttner. Hypocalcaemia. Life in the Fast Lane, 2021. https://litfl.com/hypocalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
94aacfd5-8c52-4a92-b77d-ad2d820a2671,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Buttner, Robert, and Ed Burns. Hyperkalaemia. Life in the Fast Lane. https://litfl.com/hyperkalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
2d4e7256-050c-4239-9395-881ce4ea0530,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Buttner, Robert, and Ed Burns. Hypokalaemia. Life in the Fast Lane, 2021. https://litfl.com/hypokalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
40c0d362-cd4b-468e-baef-9fd2bfc1e438,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Chhabra, Lovely, Amandeep Goyal, and Michael D. Benham. Wolff Parkinson White Syndrome. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK554437/, CC BY 4.0.",True,Text,,,,
b22b312f-5dab-40ed-8fdc-b64bd7fed1a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Custer, Adam M., Varun S. Yelamanchili, and Sarah L. Lappin. Multifocal Atrial Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459152/, CC BY 4.0.",True,Text,,,,
89ba4b59-f01a-4c55-9b65-3322ce2ad1f2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Farzam, Khashayar, and John R. Richards. Premature Ventricular Contraction. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532991/, CC BY 4.0.",True,Text,,,,
ef3218a7-5c88-4b5c-8793-cc65497917d7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Foth, Christopher, Manesh Kumar Gangwani, and Heidi Alvey. Ventricular Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532954/, CC BY 4.0.",True,Text,,,,
1d4003ac-0657-4f12-a0fe-8f4f45af2e13,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Hafeez, Yamama, and Shamai A. Grossman. Sinus Bradycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK493201/, CC BY 4.0.",True,Text,,,,
f295f292-c89b-4d7a-a13c-7091ba914d98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Harkness, Weston T., and Mary Hicks. Right Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK507872/, CC BY 4.0.",True,Text,,,,
719270d9-7e52-416f-b2ed-95d1ad83e37d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Heaton, Joseph, and Srikanth Yandrapalli. Premature Atrial Contractions. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK559204/, CC BY 4.0.",True,Text,,,,
a906dc81-bacc-4104-a892-4aafad355355,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Kashou, Anthony H., Amandeep Goyal, Tran Nguyen, and Lovely Chhabra. Atrioventricular Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459147/, CC BY 4.0.",True,Text,,,,
61801286-80c0-4ad4-ac01-b9aa94a6de86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,“Learn the Heart.” Healio. https://www.healio.com/cardiology/learn-the-heart.,True,Text,,,,
ff724b15-5d80-43bc-acc5-54d35677dbe5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Ludhwani, Dipesh, Amandeep Goyal, and Mandar Jagtap. Ventricular Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK537120/, CC BY 4.0.",True,Text,,,,
42b3b438-28e9-4ac9-8eac-c99c3a2c3e6c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Nesheiwat, Zeid, Amandeep Goyal, and Mandar Jagtap. Atrial Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK526072/, CC BY 4.0.",True,Text,,,,
b1d579cc-93ab-433e-a129-2bfb732fce3c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Pipilas, Daniel C., Bruce A. Koplan, and Leonard S. Lilly. “The Electrocardiogram.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 4. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
8ebee4d8-de14-4632-adf3-3d1caf81960c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Rodriguez Ziccardi, Mary, Amandeep Goyal, and Christopher V. Maani. Atrial Flutter. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK540985/, CC BY 4.0.",True,Text,,,,
8f8106b0-5469-470f-8ee4-20685b835bfc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-7,"Scherbak, Dmitriy, and Gregory J. Hicks. Left Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK482167/, CC BY 4.0.",True,Text,,,,
3de42e41-a332-4ad9-9ca2-a840824da3a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,USMLE,False,USMLE,,,,
013d24bd-c934-48a0-814e-ef717a3de049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
013d24bd-c934-48a0-814e-ef717a3de049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
013d24bd-c934-48a0-814e-ef717a3de049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
013d24bd-c934-48a0-814e-ef717a3de049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
013d24bd-c934-48a0-814e-ef717a3de049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
013d24bd-c934-48a0-814e-ef717a3de049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
013d24bd-c934-48a0-814e-ef717a3de049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
013d24bd-c934-48a0-814e-ef717a3de049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
013d24bd-c934-48a0-814e-ef717a3de049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
013d24bd-c934-48a0-814e-ef717a3de049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
013d24bd-c934-48a0-814e-ef717a3de049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
013d24bd-c934-48a0-814e-ef717a3de049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
013d24bd-c934-48a0-814e-ef717a3de049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
013d24bd-c934-48a0-814e-ef717a3de049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
013d24bd-c934-48a0-814e-ef717a3de049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
013d24bd-c934-48a0-814e-ef717a3de049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
013d24bd-c934-48a0-814e-ef717a3de049,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
59228581-baf5-4bd7-a77b-b5fbebf5aec4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,10q22,False,10q22,,,,
d6b74001-24b5-4096-952d-ab86e46f18d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,q24,False,q24,,,,
c3ab783d-a83a-4758-babf-2c0f4654d9c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,fibrillatory,False,fibrillatory,,,,
d25b1863-4420-4b52-bf8d-0561fe493e9f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d25b1863-4420-4b52-bf8d-0561fe493e9f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d25b1863-4420-4b52-bf8d-0561fe493e9f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d25b1863-4420-4b52-bf8d-0561fe493e9f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d25b1863-4420-4b52-bf8d-0561fe493e9f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d25b1863-4420-4b52-bf8d-0561fe493e9f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d25b1863-4420-4b52-bf8d-0561fe493e9f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d25b1863-4420-4b52-bf8d-0561fe493e9f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d25b1863-4420-4b52-bf8d-0561fe493e9f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d25b1863-4420-4b52-bf8d-0561fe493e9f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d25b1863-4420-4b52-bf8d-0561fe493e9f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d25b1863-4420-4b52-bf8d-0561fe493e9f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d25b1863-4420-4b52-bf8d-0561fe493e9f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d25b1863-4420-4b52-bf8d-0561fe493e9f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d25b1863-4420-4b52-bf8d-0561fe493e9f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d25b1863-4420-4b52-bf8d-0561fe493e9f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
d25b1863-4420-4b52-bf8d-0561fe493e9f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
84394fab-9121-4eb7-a4ba-c77697a09fc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Table 1.1: Atrial fibrillation summary.,True,fibrillatory,,,,
10adbbc6-59ba-411f-9f93-0f96658b4600,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Atrial Flutter,False,Atrial Flutter,,,,
2dcdd6f1-0179-471d-a845-750d79e0583e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
2dcdd6f1-0179-471d-a845-750d79e0583e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
2dcdd6f1-0179-471d-a845-750d79e0583e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
2dcdd6f1-0179-471d-a845-750d79e0583e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
2dcdd6f1-0179-471d-a845-750d79e0583e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
2dcdd6f1-0179-471d-a845-750d79e0583e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
2dcdd6f1-0179-471d-a845-750d79e0583e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
2dcdd6f1-0179-471d-a845-750d79e0583e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
2dcdd6f1-0179-471d-a845-750d79e0583e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
2dcdd6f1-0179-471d-a845-750d79e0583e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
2dcdd6f1-0179-471d-a845-750d79e0583e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
2dcdd6f1-0179-471d-a845-750d79e0583e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
2dcdd6f1-0179-471d-a845-750d79e0583e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
2dcdd6f1-0179-471d-a845-750d79e0583e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
2dcdd6f1-0179-471d-a845-750d79e0583e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
2dcdd6f1-0179-471d-a845-750d79e0583e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
2dcdd6f1-0179-471d-a845-750d79e0583e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
ebeba7dc-9406-44ae-8973-a9a691e268db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,macroreentrant,False,macroreentrant,,,,
2c26efc1-9bbe-48b5-bd1a-37acb5bfdc73,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,cavotricuspid,False,cavotricuspid,,,,
29315161-0716-484a-b8ae-1fa8cacadcc0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"As with atrial fibrillation, the AV node’s refractory period prevents most of the P-waves from progressing to the ventricle, but commonly the AV conduction will be 2-to-1, so with an atrial rate of 300 bpm the ventricular rate will be 150 bpm. Parasympathetic stimulation or changes in AV node refractoriness can modify how many P-waves pass into the ventricle, but the the resultant rhythm is “regularly irregular.” When the heart rate is elevated, then distinguishing flutter from fibrillation becomes challenging and slowing ventricular rate pharmaceutically (adenosine) helps the flutter waves reemerge for a definitive diagnosis to be made.",True,cavotricuspid,,,,
5ae86c31-9c4d-4e86-ac0e-bf569bbc662b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Table 1.2: Atrial flutter summary.,True,cavotricuspid,,,,
9333801d-2487-4e72-8155-721d59df85a1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Multifocal Atrial Tachycardia,False,Multifocal Atrial Tachycardia,,,,
fc009dd2-d9e3-40cf-aebc-bd7bd1ba0609,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
fc009dd2-d9e3-40cf-aebc-bd7bd1ba0609,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
fc009dd2-d9e3-40cf-aebc-bd7bd1ba0609,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
fc009dd2-d9e3-40cf-aebc-bd7bd1ba0609,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
fc009dd2-d9e3-40cf-aebc-bd7bd1ba0609,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
fc009dd2-d9e3-40cf-aebc-bd7bd1ba0609,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
fc009dd2-d9e3-40cf-aebc-bd7bd1ba0609,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
fc009dd2-d9e3-40cf-aebc-bd7bd1ba0609,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
fc009dd2-d9e3-40cf-aebc-bd7bd1ba0609,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
fc009dd2-d9e3-40cf-aebc-bd7bd1ba0609,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
fc009dd2-d9e3-40cf-aebc-bd7bd1ba0609,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
fc009dd2-d9e3-40cf-aebc-bd7bd1ba0609,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
fc009dd2-d9e3-40cf-aebc-bd7bd1ba0609,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
fc009dd2-d9e3-40cf-aebc-bd7bd1ba0609,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
fc009dd2-d9e3-40cf-aebc-bd7bd1ba0609,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
fc009dd2-d9e3-40cf-aebc-bd7bd1ba0609,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
fc009dd2-d9e3-40cf-aebc-bd7bd1ba0609,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
d6cf59de-ec9f-448f-a716-5210e309f281,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"MAT frequently occurs in the setting of severe lung disease and, more specifically, during an exacerbation of lung disease. This rhythm is benign, and once the underlying lung disease is treated, it should resolve.",True,Multifocal Atrial Tachycardia,,,,
fcefe789-b32c-4f63-aeda-91f4f3649098,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Table 1.3: MAT summary.,True,Multifocal Atrial Tachycardia,,,,
4c4ecfe0-7521-4783-8728-81a7a7bb30a4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Premature Atrial Contraction,False,Premature Atrial Contraction,,,,
2d3f3892-6190-4983-967f-0df5f9530bd6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A premature atrial contraction (PAC) is generated by a depolarization instigated outside of the SA node. This produces an extra P-wave, and consequently a shortening from previous P-P intervals is seen. The aberrant P-wave also has a different morphology from a sinus P-wave because of its different anatomical origin.",True,Premature Atrial Contraction,,,,
7d7e6b44-7da8-493b-a47d-45c965314462,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d7e6b44-7da8-493b-a47d-45c965314462,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d7e6b44-7da8-493b-a47d-45c965314462,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d7e6b44-7da8-493b-a47d-45c965314462,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d7e6b44-7da8-493b-a47d-45c965314462,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d7e6b44-7da8-493b-a47d-45c965314462,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d7e6b44-7da8-493b-a47d-45c965314462,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d7e6b44-7da8-493b-a47d-45c965314462,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d7e6b44-7da8-493b-a47d-45c965314462,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d7e6b44-7da8-493b-a47d-45c965314462,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d7e6b44-7da8-493b-a47d-45c965314462,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d7e6b44-7da8-493b-a47d-45c965314462,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d7e6b44-7da8-493b-a47d-45c965314462,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d7e6b44-7da8-493b-a47d-45c965314462,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d7e6b44-7da8-493b-a47d-45c965314462,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d7e6b44-7da8-493b-a47d-45c965314462,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
7d7e6b44-7da8-493b-a47d-45c965314462,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
99bf6c0d-8b6f-4cd0-9c6c-5147acc3b2f9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"If a PAC occurs when the AV node has not yet recovered from its refractory period, the PAC will fail to conduct to the ventricles; meaning the PAC will not be followed by a QRS complex or the ectopic P-R interval will be prolonged. The ECG will show a premature, ectopic P-wave and then no QRS complex afterward. When this occurs along with bigeminy, the ECG can appear as if there is sinus bradycardia.",True,Premature Atrial Contraction,,,,
3603dc94-c7e9-4c02-a65a-d53d6d9a2ac1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Table 1.4: PAC summary.,True,Premature Atrial Contraction,,,,
054042d7-a1f0-48c2-ae30-0f49254dff27,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Sinus Bradycardia,False,Sinus Bradycardia,,,,
28759277-e8e6-419c-8633-6f8fc3cf44c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Sinus bradycardia denotes a sinus rhythm below 60 bpm. Otherwise the ECG waveform is normal on an ECG with an upright P-wave in lead II preceding every QRS complex. There are many intrinsic causes associated with the heart itself, as well as extrinsic causes, some of which are listed table 1.5. Sinus bradycardia is usually asymptomatic as rates of 40–50 bpm can maintain hemodynamic stability. Rates below this can produce symptoms of fatigue, dizziness, and dyspnea on exertion.",True,Sinus Bradycardia,,,,
594c9136-eba7-4955-8b71-261b03166dd0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Table 1.5: Intrinsic and extrinsic causes associated with the heart.,True,Sinus Bradycardia,,,,
d464753e-f4d4-4ae7-aca6-708ac490079a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Table 1.6: Sinus bradycardia summary.,True,Sinus Bradycardia,,,,
4d113c36-15ff-460a-a9e7-277ab9544c9d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Premature Ventricular Contractions,False,Premature Ventricular Contractions,,,,
f8452fc4-dbb1-4cba-b864-73947850dc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
f8452fc4-dbb1-4cba-b864-73947850dc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
f8452fc4-dbb1-4cba-b864-73947850dc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
f8452fc4-dbb1-4cba-b864-73947850dc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
f8452fc4-dbb1-4cba-b864-73947850dc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
f8452fc4-dbb1-4cba-b864-73947850dc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
f8452fc4-dbb1-4cba-b864-73947850dc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
f8452fc4-dbb1-4cba-b864-73947850dc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
f8452fc4-dbb1-4cba-b864-73947850dc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
f8452fc4-dbb1-4cba-b864-73947850dc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
f8452fc4-dbb1-4cba-b864-73947850dc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
f8452fc4-dbb1-4cba-b864-73947850dc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
f8452fc4-dbb1-4cba-b864-73947850dc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
f8452fc4-dbb1-4cba-b864-73947850dc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
f8452fc4-dbb1-4cba-b864-73947850dc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
f8452fc4-dbb1-4cba-b864-73947850dc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
f8452fc4-dbb1-4cba-b864-73947850dc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
c272d7b6-2664-4b50-843a-7f1af6d39ffe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Table 1.7: PVC summary.,True,Premature Ventricular Contractions,,,,
b2aed863-9005-4cb9-836b-881ff11da088,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Ventricular Tachycardia,False,Ventricular Tachycardia,,,,
a5599454-c672-434e-ade4-18754e873156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Ventricular tachycardia (VT) is caused by reentry currents being established in the ventricular myocardium or groups of ventricular myocytes that have aberrant electrical behavior. As such, VT is usually caused by underlying cardiac disease.",True,Ventricular Tachycardia,,,,
d0d42d65-3b34-49bb-8fc2-c525308104ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Like a PVC, the aberrant depolarizations do not follow the normal conduction pathways so are wide (>120 msecs), but unlike a PVC, VT involves a ventricular rate >100 bpm. With disorganized contractility and reduced filling time, VT can lead to hemodynamic instability and severe hypotension—hence it is life threatening.",True,Ventricular Tachycardia,,,,
449adcc4-5d0e-4678-a4b4-9023e268c137,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The QRS morphology in VT is highly variable between patients and depends on where the arrhythmia originates. Consequently there are several ways to classify VT based on duration, symptoms, QRS morphology, rate, and origin.",True,Ventricular Tachycardia,,,,
7b2a5bf5-5ba9-42a9-b134-088142700093,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Sustained VT is any VT that lasts for more than 30 seconds or is symptomatic. Nonsustained VT lasts for less than 30 seconds and is asymptomatic.,True,Ventricular Tachycardia,,,,
30298e56-9a40-4fca-baab-cd9c50bc456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
30298e56-9a40-4fca-baab-cd9c50bc456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
30298e56-9a40-4fca-baab-cd9c50bc456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
30298e56-9a40-4fca-baab-cd9c50bc456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
30298e56-9a40-4fca-baab-cd9c50bc456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
30298e56-9a40-4fca-baab-cd9c50bc456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
30298e56-9a40-4fca-baab-cd9c50bc456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
30298e56-9a40-4fca-baab-cd9c50bc456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
30298e56-9a40-4fca-baab-cd9c50bc456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
30298e56-9a40-4fca-baab-cd9c50bc456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
30298e56-9a40-4fca-baab-cd9c50bc456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
30298e56-9a40-4fca-baab-cd9c50bc456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
30298e56-9a40-4fca-baab-cd9c50bc456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
30298e56-9a40-4fca-baab-cd9c50bc456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
30298e56-9a40-4fca-baab-cd9c50bc456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
30298e56-9a40-4fca-baab-cd9c50bc456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
30298e56-9a40-4fca-baab-cd9c50bc456b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
a527b6ba-804e-4092-a85e-9f54a63fcdc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a527b6ba-804e-4092-a85e-9f54a63fcdc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a527b6ba-804e-4092-a85e-9f54a63fcdc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a527b6ba-804e-4092-a85e-9f54a63fcdc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a527b6ba-804e-4092-a85e-9f54a63fcdc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a527b6ba-804e-4092-a85e-9f54a63fcdc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a527b6ba-804e-4092-a85e-9f54a63fcdc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a527b6ba-804e-4092-a85e-9f54a63fcdc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a527b6ba-804e-4092-a85e-9f54a63fcdc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a527b6ba-804e-4092-a85e-9f54a63fcdc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a527b6ba-804e-4092-a85e-9f54a63fcdc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a527b6ba-804e-4092-a85e-9f54a63fcdc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a527b6ba-804e-4092-a85e-9f54a63fcdc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a527b6ba-804e-4092-a85e-9f54a63fcdc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a527b6ba-804e-4092-a85e-9f54a63fcdc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a527b6ba-804e-4092-a85e-9f54a63fcdc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
a527b6ba-804e-4092-a85e-9f54a63fcdc4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
13428588-2abe-481a-946d-c8b2964f278a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Torsades de pointes is associated with a prolonged QT interval (>600 msecs) that helps distinguish it from other forms of polymorphous VT. The longer QT interval can be caused by ionic abnormalities that reduce the repolarizing current of Phase 3 of the cardiac action potential. This makes the myocardium susceptible to early after-depolarizations—the trigger for torsades de pointes. These after-depolarizations do not happen uniformly across the myocardium and are more common in endocardial tissue where the repolarization currents are slower. So torsades de pointes arises from the after-depolarizations causing reentry currents in neighboring tissue.,True,Ventricular Tachycardia,,,,
caa2f999-2260-4057-973e-d8854d869543,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Both common garden variety VTs and torsades de pointes can progress to ventricular fibrillation.,True,Ventricular Tachycardia,,,,
2bc37807-4621-456c-8e8d-2bebdcc8ca99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Table 1.8: VT summary.,True,Ventricular Tachycardia,,,,
fb23783e-540c-4c3d-bc6e-6a3857dfdfad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Ventricular Fibrillation,False,Ventricular Fibrillation,,,,
b1bd2654-de90-4bcf-9ad2-f5329d3d3cf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Ventricular fibrillation (VF) occurs when the ventricular rate exceeds 400 bpm. The disorganized and uncoordinated contraction of the myocardium causes cardiac output to fall to catastrophic levels. Rates of survival for out-of-hospital VF are low.,True,Ventricular Fibrillation,,,,
0f6e4ab9-1bce-4b04-bfed-3b0717ab54b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0f6e4ab9-1bce-4b04-bfed-3b0717ab54b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0f6e4ab9-1bce-4b04-bfed-3b0717ab54b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0f6e4ab9-1bce-4b04-bfed-3b0717ab54b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0f6e4ab9-1bce-4b04-bfed-3b0717ab54b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0f6e4ab9-1bce-4b04-bfed-3b0717ab54b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0f6e4ab9-1bce-4b04-bfed-3b0717ab54b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0f6e4ab9-1bce-4b04-bfed-3b0717ab54b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0f6e4ab9-1bce-4b04-bfed-3b0717ab54b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0f6e4ab9-1bce-4b04-bfed-3b0717ab54b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0f6e4ab9-1bce-4b04-bfed-3b0717ab54b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0f6e4ab9-1bce-4b04-bfed-3b0717ab54b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0f6e4ab9-1bce-4b04-bfed-3b0717ab54b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0f6e4ab9-1bce-4b04-bfed-3b0717ab54b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0f6e4ab9-1bce-4b04-bfed-3b0717ab54b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0f6e4ab9-1bce-4b04-bfed-3b0717ab54b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
0f6e4ab9-1bce-4b04-bfed-3b0717ab54b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
b20d4f1e-e55d-4042-9c63-dfe180884cc3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Table 1.9: VF summary.,True,Ventricular Fibrillation,,,,
25c657f1-e27b-493a-99a5-27122cb13dc6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,First-Degree Atrioventricular Block,False,First-Degree Atrioventricular Block,,,,
d09ec942-f5ca-466f-a91d-b8847ea31d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d09ec942-f5ca-466f-a91d-b8847ea31d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d09ec942-f5ca-466f-a91d-b8847ea31d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d09ec942-f5ca-466f-a91d-b8847ea31d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d09ec942-f5ca-466f-a91d-b8847ea31d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d09ec942-f5ca-466f-a91d-b8847ea31d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d09ec942-f5ca-466f-a91d-b8847ea31d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d09ec942-f5ca-466f-a91d-b8847ea31d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d09ec942-f5ca-466f-a91d-b8847ea31d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d09ec942-f5ca-466f-a91d-b8847ea31d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d09ec942-f5ca-466f-a91d-b8847ea31d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d09ec942-f5ca-466f-a91d-b8847ea31d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d09ec942-f5ca-466f-a91d-b8847ea31d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d09ec942-f5ca-466f-a91d-b8847ea31d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d09ec942-f5ca-466f-a91d-b8847ea31d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d09ec942-f5ca-466f-a91d-b8847ea31d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d09ec942-f5ca-466f-a91d-b8847ea31d29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
69fb21c4-eb5c-4220-8c8e-a9a667021ba6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
69fb21c4-eb5c-4220-8c8e-a9a667021ba6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
69fb21c4-eb5c-4220-8c8e-a9a667021ba6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
69fb21c4-eb5c-4220-8c8e-a9a667021ba6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
69fb21c4-eb5c-4220-8c8e-a9a667021ba6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
69fb21c4-eb5c-4220-8c8e-a9a667021ba6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
69fb21c4-eb5c-4220-8c8e-a9a667021ba6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
69fb21c4-eb5c-4220-8c8e-a9a667021ba6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
69fb21c4-eb5c-4220-8c8e-a9a667021ba6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
69fb21c4-eb5c-4220-8c8e-a9a667021ba6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
69fb21c4-eb5c-4220-8c8e-a9a667021ba6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
69fb21c4-eb5c-4220-8c8e-a9a667021ba6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
69fb21c4-eb5c-4220-8c8e-a9a667021ba6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
69fb21c4-eb5c-4220-8c8e-a9a667021ba6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
69fb21c4-eb5c-4220-8c8e-a9a667021ba6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
69fb21c4-eb5c-4220-8c8e-a9a667021ba6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
69fb21c4-eb5c-4220-8c8e-a9a667021ba6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
c3816f02-05df-4e9d-adc6-a763bf50ebc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Table 1.10: First-degree block summary.,True,First-Degree Atrioventricular Block,,,,
b82d7988-9755-443a-8c38-5a4349a1e32e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Second-Degree Atrioventricular Block,False,Second-Degree Atrioventricular Block,,,,
a5d110ac-0432-44e9-89f3-dddfd0d7349b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A second-degree atrioventricular block also has changes in P-R interval, but it starts to show failure of the P-wave to propagate a QRS complex every time (i.e., intermittently the depolarization fails to reach the ventricles). The pattern of missed ventricular depolarizations, or blocked P-waves, is often very regular and described as a ratio of P-waves to QRS complex. The way in which the P-R interval changes in relation to the blocked P-waves produces subclassifications of second-degree blocks, Mobitz I and II.",True,Second-Degree Atrioventricular Block,,,,
89af0525-a47a-4fe4-b644-c5b1164e8988,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
89af0525-a47a-4fe4-b644-c5b1164e8988,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
89af0525-a47a-4fe4-b644-c5b1164e8988,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
89af0525-a47a-4fe4-b644-c5b1164e8988,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
89af0525-a47a-4fe4-b644-c5b1164e8988,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
89af0525-a47a-4fe4-b644-c5b1164e8988,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
89af0525-a47a-4fe4-b644-c5b1164e8988,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
89af0525-a47a-4fe4-b644-c5b1164e8988,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
89af0525-a47a-4fe4-b644-c5b1164e8988,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
89af0525-a47a-4fe4-b644-c5b1164e8988,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
89af0525-a47a-4fe4-b644-c5b1164e8988,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
89af0525-a47a-4fe4-b644-c5b1164e8988,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
89af0525-a47a-4fe4-b644-c5b1164e8988,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
89af0525-a47a-4fe4-b644-c5b1164e8988,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
89af0525-a47a-4fe4-b644-c5b1164e8988,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
89af0525-a47a-4fe4-b644-c5b1164e8988,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
89af0525-a47a-4fe4-b644-c5b1164e8988,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
688145ca-07f8-498c-9160-eeb8bf71bf1e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
688145ca-07f8-498c-9160-eeb8bf71bf1e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
688145ca-07f8-498c-9160-eeb8bf71bf1e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
688145ca-07f8-498c-9160-eeb8bf71bf1e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
688145ca-07f8-498c-9160-eeb8bf71bf1e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
688145ca-07f8-498c-9160-eeb8bf71bf1e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
688145ca-07f8-498c-9160-eeb8bf71bf1e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
688145ca-07f8-498c-9160-eeb8bf71bf1e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
688145ca-07f8-498c-9160-eeb8bf71bf1e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
688145ca-07f8-498c-9160-eeb8bf71bf1e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
688145ca-07f8-498c-9160-eeb8bf71bf1e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
688145ca-07f8-498c-9160-eeb8bf71bf1e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
688145ca-07f8-498c-9160-eeb8bf71bf1e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
688145ca-07f8-498c-9160-eeb8bf71bf1e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
688145ca-07f8-498c-9160-eeb8bf71bf1e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
688145ca-07f8-498c-9160-eeb8bf71bf1e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
688145ca-07f8-498c-9160-eeb8bf71bf1e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
802933d8-2771-4f6e-bcde-772fca205553,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Table 1.11: Second-degree block summary.,True,Second-Degree Atrioventricular Block,,,,
2d44dde8-32e5-4db6-b796-a277251f7cba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Third-Degree Atrioventricular Block,False,Third-Degree Atrioventricular Block,,,,
8864c4d0-6ad1-4323-b92f-0979266dcb31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8864c4d0-6ad1-4323-b92f-0979266dcb31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8864c4d0-6ad1-4323-b92f-0979266dcb31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8864c4d0-6ad1-4323-b92f-0979266dcb31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8864c4d0-6ad1-4323-b92f-0979266dcb31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8864c4d0-6ad1-4323-b92f-0979266dcb31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8864c4d0-6ad1-4323-b92f-0979266dcb31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8864c4d0-6ad1-4323-b92f-0979266dcb31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8864c4d0-6ad1-4323-b92f-0979266dcb31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8864c4d0-6ad1-4323-b92f-0979266dcb31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8864c4d0-6ad1-4323-b92f-0979266dcb31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8864c4d0-6ad1-4323-b92f-0979266dcb31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8864c4d0-6ad1-4323-b92f-0979266dcb31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8864c4d0-6ad1-4323-b92f-0979266dcb31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8864c4d0-6ad1-4323-b92f-0979266dcb31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8864c4d0-6ad1-4323-b92f-0979266dcb31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
8864c4d0-6ad1-4323-b92f-0979266dcb31,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
a04a55b6-a994-4d4e-b73f-b6ff80fa03e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Table 1.12: Third-degree block summary.,True,Third-Degree Atrioventricular Block,,,,
c9f4a43a-554f-4caa-bc25-1fce5ba0dc6b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Left Bundle Branch Block,False,Left Bundle Branch Block,,,,
5ee3fd6d-30c2-47d7-8f48-082b8ccd1772,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"A left bundle branch block (LBBB) is generated when the conductivity of the His-Purkinje system in the left ventricle is compromised, either through damage or disease. The ECG changes, and criteria for LBBB relate to these changes in conductivity and the left-side location.",True,Left Bundle Branch Block,,,,
ba4ee2d2-f731-4378-93e5-142d52b405a2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ba4ee2d2-f731-4378-93e5-142d52b405a2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ba4ee2d2-f731-4378-93e5-142d52b405a2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ba4ee2d2-f731-4378-93e5-142d52b405a2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ba4ee2d2-f731-4378-93e5-142d52b405a2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ba4ee2d2-f731-4378-93e5-142d52b405a2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ba4ee2d2-f731-4378-93e5-142d52b405a2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ba4ee2d2-f731-4378-93e5-142d52b405a2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ba4ee2d2-f731-4378-93e5-142d52b405a2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ba4ee2d2-f731-4378-93e5-142d52b405a2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ba4ee2d2-f731-4378-93e5-142d52b405a2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ba4ee2d2-f731-4378-93e5-142d52b405a2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ba4ee2d2-f731-4378-93e5-142d52b405a2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ba4ee2d2-f731-4378-93e5-142d52b405a2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ba4ee2d2-f731-4378-93e5-142d52b405a2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ba4ee2d2-f731-4378-93e5-142d52b405a2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
ba4ee2d2-f731-4378-93e5-142d52b405a2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
e870c076-26f6-47bb-b6c2-455add033634,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The lateral leads (I, V5, and V6) normally show a downward deflecting Q-wave as normal septal deflection initially occurs left-to-right (i.e., away from the lateral leads). In LBBB the change in direction to right-to-left, plus the longer duration, eliminates the Q-wave from the lateral leads, and Q-waves will be small in aVL.",True,Left Bundle Branch Block,,,,
41a1078b-d0dc-4e7e-9ce0-d0933a4dc361,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
41a1078b-d0dc-4e7e-9ce0-d0933a4dc361,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
41a1078b-d0dc-4e7e-9ce0-d0933a4dc361,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
41a1078b-d0dc-4e7e-9ce0-d0933a4dc361,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
41a1078b-d0dc-4e7e-9ce0-d0933a4dc361,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
41a1078b-d0dc-4e7e-9ce0-d0933a4dc361,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
41a1078b-d0dc-4e7e-9ce0-d0933a4dc361,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
41a1078b-d0dc-4e7e-9ce0-d0933a4dc361,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
41a1078b-d0dc-4e7e-9ce0-d0933a4dc361,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
41a1078b-d0dc-4e7e-9ce0-d0933a4dc361,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
41a1078b-d0dc-4e7e-9ce0-d0933a4dc361,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
41a1078b-d0dc-4e7e-9ce0-d0933a4dc361,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
41a1078b-d0dc-4e7e-9ce0-d0933a4dc361,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
41a1078b-d0dc-4e7e-9ce0-d0933a4dc361,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
41a1078b-d0dc-4e7e-9ce0-d0933a4dc361,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
41a1078b-d0dc-4e7e-9ce0-d0933a4dc361,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
41a1078b-d0dc-4e7e-9ce0-d0933a4dc361,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
87bb8601-3bcc-4cc0-80f5-3255481aff6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
87bb8601-3bcc-4cc0-80f5-3255481aff6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
87bb8601-3bcc-4cc0-80f5-3255481aff6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
87bb8601-3bcc-4cc0-80f5-3255481aff6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
87bb8601-3bcc-4cc0-80f5-3255481aff6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
87bb8601-3bcc-4cc0-80f5-3255481aff6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
87bb8601-3bcc-4cc0-80f5-3255481aff6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
87bb8601-3bcc-4cc0-80f5-3255481aff6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
87bb8601-3bcc-4cc0-80f5-3255481aff6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
87bb8601-3bcc-4cc0-80f5-3255481aff6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
87bb8601-3bcc-4cc0-80f5-3255481aff6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
87bb8601-3bcc-4cc0-80f5-3255481aff6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
87bb8601-3bcc-4cc0-80f5-3255481aff6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
87bb8601-3bcc-4cc0-80f5-3255481aff6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
87bb8601-3bcc-4cc0-80f5-3255481aff6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
87bb8601-3bcc-4cc0-80f5-3255481aff6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
87bb8601-3bcc-4cc0-80f5-3255481aff6a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
7659846c-0b23-4e23-9819-b893ac5c1aca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Table 1.13: LBBB summary.,True,Left Bundle Branch Block,,,,
af7772f3-3fd3-416b-955e-a8837748fbe3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Right Bundle Branch Block,False,Right Bundle Branch Block,,,,
6ce9769f-ed97-49c9-881e-b1c461c0a0c3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The causes and manifestations of a right bundle branch block (RBBB) bear some similarities to those described for LBBB, but of course this time its depolarization of the right ventricle is delayed. Causes of RBBB include ischemic heart disease again as well as other myocardial diseases, but pulmonary issues such as pulmonary embolism and cor pulmonale can be added to the list.",True,Right Bundle Branch Block,,,,
9f02f31e-dcc8-43b5-8f9c-223bf245fcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
9f02f31e-dcc8-43b5-8f9c-223bf245fcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
9f02f31e-dcc8-43b5-8f9c-223bf245fcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
9f02f31e-dcc8-43b5-8f9c-223bf245fcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
9f02f31e-dcc8-43b5-8f9c-223bf245fcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
9f02f31e-dcc8-43b5-8f9c-223bf245fcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
9f02f31e-dcc8-43b5-8f9c-223bf245fcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
9f02f31e-dcc8-43b5-8f9c-223bf245fcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
9f02f31e-dcc8-43b5-8f9c-223bf245fcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
9f02f31e-dcc8-43b5-8f9c-223bf245fcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
9f02f31e-dcc8-43b5-8f9c-223bf245fcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
9f02f31e-dcc8-43b5-8f9c-223bf245fcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
9f02f31e-dcc8-43b5-8f9c-223bf245fcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
9f02f31e-dcc8-43b5-8f9c-223bf245fcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
9f02f31e-dcc8-43b5-8f9c-223bf245fcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
9f02f31e-dcc8-43b5-8f9c-223bf245fcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
9f02f31e-dcc8-43b5-8f9c-223bf245fcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
9b6214ac-3591-472d-aedc-58ddcc104034,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Table 1.14: RBBB summary.,True,Right Bundle Branch Block,,,,
f127d869-1d8a-4ce4-9cdc-fb50506d91f1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Wolff-Parkinson-White Syndrome,False,Wolff-Parkinson-White Syndrome,,,,
3ec58944-b8f2-4992-b0b5-10a232ff479f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Normally the only electrical connection between the atria and the ventricles is the AV node. Otherwise the fibrous skeleton of the heart electrically insulates the atria from the ventricles. In Wolff-Parkinson-White (WPW) syndrome, that insulation is incomplete, and an “accessory pathway” connects the electrical system of the atria directly to the ventricles. If you think of the AV node as a bridge over the fibrous wall with regulated access, the accessory pathway is like a pathological tunnel under it with no regulation.",True,Wolff-Parkinson-White Syndrome,,,,
43650c15-fdec-4fd8-9699-07f4c46945b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
43650c15-fdec-4fd8-9699-07f4c46945b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
43650c15-fdec-4fd8-9699-07f4c46945b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
43650c15-fdec-4fd8-9699-07f4c46945b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
43650c15-fdec-4fd8-9699-07f4c46945b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
43650c15-fdec-4fd8-9699-07f4c46945b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
43650c15-fdec-4fd8-9699-07f4c46945b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
43650c15-fdec-4fd8-9699-07f4c46945b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
43650c15-fdec-4fd8-9699-07f4c46945b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
43650c15-fdec-4fd8-9699-07f4c46945b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
43650c15-fdec-4fd8-9699-07f4c46945b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
43650c15-fdec-4fd8-9699-07f4c46945b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
43650c15-fdec-4fd8-9699-07f4c46945b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
43650c15-fdec-4fd8-9699-07f4c46945b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
43650c15-fdec-4fd8-9699-07f4c46945b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
43650c15-fdec-4fd8-9699-07f4c46945b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
43650c15-fdec-4fd8-9699-07f4c46945b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c5ffacf5-8a32-4029-b927-3539a0c77c74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"WPW syndrome is often asymptomatic, and patients do not require immediate treatment. However, if atrial fibrillation occurs in a WPW patient, the accessory pathway can allow the atrial fibrillation waves through to the ventricle (with no AV nodal refractory period to prevent them). Consequently a high ventricular rate is seen, and the risk of ventricular fibrillation being established means immediate clinical attention is required.",True,Wolff-Parkinson-White Syndrome,,,,
50febfab-d98e-424c-97f2-2c829f2f99fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Hyper- and Hypocalcemia,False,Hyper- and Hypocalcemia,,,,
e1e86e1c-5683-47b2-a78b-12b9c360540d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e1e86e1c-5683-47b2-a78b-12b9c360540d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e1e86e1c-5683-47b2-a78b-12b9c360540d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e1e86e1c-5683-47b2-a78b-12b9c360540d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e1e86e1c-5683-47b2-a78b-12b9c360540d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e1e86e1c-5683-47b2-a78b-12b9c360540d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e1e86e1c-5683-47b2-a78b-12b9c360540d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e1e86e1c-5683-47b2-a78b-12b9c360540d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e1e86e1c-5683-47b2-a78b-12b9c360540d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e1e86e1c-5683-47b2-a78b-12b9c360540d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e1e86e1c-5683-47b2-a78b-12b9c360540d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e1e86e1c-5683-47b2-a78b-12b9c360540d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e1e86e1c-5683-47b2-a78b-12b9c360540d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e1e86e1c-5683-47b2-a78b-12b9c360540d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e1e86e1c-5683-47b2-a78b-12b9c360540d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e1e86e1c-5683-47b2-a78b-12b9c360540d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e1e86e1c-5683-47b2-a78b-12b9c360540d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e4fb365d-2700-4b37-bf75-e0893f842a5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
e4fb365d-2700-4b37-bf75-e0893f842a5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
e4fb365d-2700-4b37-bf75-e0893f842a5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
e4fb365d-2700-4b37-bf75-e0893f842a5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
e4fb365d-2700-4b37-bf75-e0893f842a5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
e4fb365d-2700-4b37-bf75-e0893f842a5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
e4fb365d-2700-4b37-bf75-e0893f842a5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
e4fb365d-2700-4b37-bf75-e0893f842a5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
e4fb365d-2700-4b37-bf75-e0893f842a5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
e4fb365d-2700-4b37-bf75-e0893f842a5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
e4fb365d-2700-4b37-bf75-e0893f842a5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
e4fb365d-2700-4b37-bf75-e0893f842a5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
e4fb365d-2700-4b37-bf75-e0893f842a5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
e4fb365d-2700-4b37-bf75-e0893f842a5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
e4fb365d-2700-4b37-bf75-e0893f842a5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
e4fb365d-2700-4b37-bf75-e0893f842a5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
e4fb365d-2700-4b37-bf75-e0893f842a5e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
c72f0722-5809-41d5-8779-1734c87855a1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Table 1.16: Hyper- and hypocalcemia summary.,True,Hyper- and Hypocalcemia,,,,
62e33181-b314-48d7-82df-14086fee20ef,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Hyper- and Hypokalemia,False,Hyper- and Hypokalemia,,,,
5faf8f36-4091-4f5b-9939-2dbd6c6096b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"The pathophysiology is not as simple as changes in extracellular K+ changing the electrochemical gradient for K+. Because of potassium’s role in maintaining the resting membrane potential, shifts in extracellular potassium can also influence the activity of Na+ and Ca++ channels.",True,Hyper- and Hypokalemia,,,,
9adf23a5-dd78-4c6b-acb0-b3d16d488f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
9adf23a5-dd78-4c6b-acb0-b3d16d488f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
9adf23a5-dd78-4c6b-acb0-b3d16d488f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
9adf23a5-dd78-4c6b-acb0-b3d16d488f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
9adf23a5-dd78-4c6b-acb0-b3d16d488f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
9adf23a5-dd78-4c6b-acb0-b3d16d488f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
9adf23a5-dd78-4c6b-acb0-b3d16d488f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
9adf23a5-dd78-4c6b-acb0-b3d16d488f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
9adf23a5-dd78-4c6b-acb0-b3d16d488f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
9adf23a5-dd78-4c6b-acb0-b3d16d488f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
9adf23a5-dd78-4c6b-acb0-b3d16d488f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
9adf23a5-dd78-4c6b-acb0-b3d16d488f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
9adf23a5-dd78-4c6b-acb0-b3d16d488f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
9adf23a5-dd78-4c6b-acb0-b3d16d488f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
9adf23a5-dd78-4c6b-acb0-b3d16d488f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
9adf23a5-dd78-4c6b-acb0-b3d16d488f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
9adf23a5-dd78-4c6b-acb0-b3d16d488f3f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
638c8d88-1511-49e4-b15c-cc5cdb68caf5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"As hypokalemia also inhibits Na+-K+ ATPase, Na+ accumulates inside the cell. This in turn leads to an accumulation of Ca++ because of a subsequent failure of the Na+-Ca++ exchanger. Extended presence of these two positive ions inside the myocyte prolongs the action potential and may manifest as an increased width and amplitude of the P-wave.",True,Hyper- and Hypokalemia,,,,
0d3ef97a-66e4-444f-9405-c624ed78fc07,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"As hypokalemia worsens, the problems with K+ conductance and repolarization increase, and the myocardium becomes susceptible to early after-depolarization (EAD) arrhythmias.",True,Hyper- and Hypokalemia,,,,
acf868f9-8544-4d95-9cfc-1aca1711cb98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
acf868f9-8544-4d95-9cfc-1aca1711cb98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
acf868f9-8544-4d95-9cfc-1aca1711cb98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
acf868f9-8544-4d95-9cfc-1aca1711cb98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
acf868f9-8544-4d95-9cfc-1aca1711cb98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
acf868f9-8544-4d95-9cfc-1aca1711cb98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
acf868f9-8544-4d95-9cfc-1aca1711cb98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
acf868f9-8544-4d95-9cfc-1aca1711cb98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
acf868f9-8544-4d95-9cfc-1aca1711cb98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
acf868f9-8544-4d95-9cfc-1aca1711cb98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
acf868f9-8544-4d95-9cfc-1aca1711cb98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
acf868f9-8544-4d95-9cfc-1aca1711cb98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
acf868f9-8544-4d95-9cfc-1aca1711cb98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
acf868f9-8544-4d95-9cfc-1aca1711cb98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
acf868f9-8544-4d95-9cfc-1aca1711cb98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
acf868f9-8544-4d95-9cfc-1aca1711cb98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
acf868f9-8544-4d95-9cfc-1aca1711cb98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
7f80ae2c-5b0e-4f4f-ba2a-a1562f6ba72e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7f80ae2c-5b0e-4f4f-ba2a-a1562f6ba72e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7f80ae2c-5b0e-4f4f-ba2a-a1562f6ba72e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7f80ae2c-5b0e-4f4f-ba2a-a1562f6ba72e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7f80ae2c-5b0e-4f4f-ba2a-a1562f6ba72e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7f80ae2c-5b0e-4f4f-ba2a-a1562f6ba72e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7f80ae2c-5b0e-4f4f-ba2a-a1562f6ba72e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7f80ae2c-5b0e-4f4f-ba2a-a1562f6ba72e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7f80ae2c-5b0e-4f4f-ba2a-a1562f6ba72e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7f80ae2c-5b0e-4f4f-ba2a-a1562f6ba72e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7f80ae2c-5b0e-4f4f-ba2a-a1562f6ba72e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7f80ae2c-5b0e-4f4f-ba2a-a1562f6ba72e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7f80ae2c-5b0e-4f4f-ba2a-a1562f6ba72e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7f80ae2c-5b0e-4f4f-ba2a-a1562f6ba72e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7f80ae2c-5b0e-4f4f-ba2a-a1562f6ba72e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7f80ae2c-5b0e-4f4f-ba2a-a1562f6ba72e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
7f80ae2c-5b0e-4f4f-ba2a-a1562f6ba72e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
8f513ade-275b-4451-94ba-be721a8a5cee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
8f513ade-275b-4451-94ba-be721a8a5cee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
8f513ade-275b-4451-94ba-be721a8a5cee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
8f513ade-275b-4451-94ba-be721a8a5cee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
8f513ade-275b-4451-94ba-be721a8a5cee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
8f513ade-275b-4451-94ba-be721a8a5cee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
8f513ade-275b-4451-94ba-be721a8a5cee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
8f513ade-275b-4451-94ba-be721a8a5cee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
8f513ade-275b-4451-94ba-be721a8a5cee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
8f513ade-275b-4451-94ba-be721a8a5cee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
8f513ade-275b-4451-94ba-be721a8a5cee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
8f513ade-275b-4451-94ba-be721a8a5cee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
8f513ade-275b-4451-94ba-be721a8a5cee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
8f513ade-275b-4451-94ba-be721a8a5cee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
8f513ade-275b-4451-94ba-be721a8a5cee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
8f513ade-275b-4451-94ba-be721a8a5cee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
8f513ade-275b-4451-94ba-be721a8a5cee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
95d174af-a42c-4439-88f5-81131f5f0b23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
95d174af-a42c-4439-88f5-81131f5f0b23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
95d174af-a42c-4439-88f5-81131f5f0b23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
95d174af-a42c-4439-88f5-81131f5f0b23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
95d174af-a42c-4439-88f5-81131f5f0b23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
95d174af-a42c-4439-88f5-81131f5f0b23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
95d174af-a42c-4439-88f5-81131f5f0b23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
95d174af-a42c-4439-88f5-81131f5f0b23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
95d174af-a42c-4439-88f5-81131f5f0b23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
95d174af-a42c-4439-88f5-81131f5f0b23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
95d174af-a42c-4439-88f5-81131f5f0b23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
95d174af-a42c-4439-88f5-81131f5f0b23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
95d174af-a42c-4439-88f5-81131f5f0b23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
95d174af-a42c-4439-88f5-81131f5f0b23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
95d174af-a42c-4439-88f5-81131f5f0b23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
95d174af-a42c-4439-88f5-81131f5f0b23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
95d174af-a42c-4439-88f5-81131f5f0b23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
aec92a4e-9be8-4ae0-9b69-e8a84ae1c4ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Table 1.17: Hypo- and hyperkalemia summary.,True,Hyper- and Hypokalemia,,,,
f5d426e3-2173-4166-9de4-91ac452612eb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"References, resources, and further reading",False,"References, resources, and further reading",,,,
483e143a-2844-46c0-8276-f61cfe84f164,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,Text,False,Text,,,,
e41a8f18-bf9e-4679-8ff2-0ae6dbac553a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Burns, Ed, and Robert Buttner. Hypercalcaemia. Lift in the Fast Lane, 2021. https://litfl.com/hypercalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
1e14efad-44d3-4433-9410-fc29cf845288,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Burns, Ed, and Robert Buttner. Hypocalcaemia. Life in the Fast Lane, 2021. https://litfl.com/hypocalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
a0705e04-a92f-404c-b09e-70867153b108,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Buttner, Robert, and Ed Burns. Hyperkalaemia. Life in the Fast Lane. https://litfl.com/hyperkalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
083c91e3-9d66-4691-a9d6-9326f98cfc73,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Buttner, Robert, and Ed Burns. Hypokalaemia. Life in the Fast Lane, 2021. https://litfl.com/hypokalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
d6d04388-0ea7-4d53-b3ba-163eb9764ca8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Chhabra, Lovely, Amandeep Goyal, and Michael D. Benham. Wolff Parkinson White Syndrome. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK554437/, CC BY 4.0.",True,Text,,,,
e178b22c-2cdd-49a8-b713-100c3c641960,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Custer, Adam M., Varun S. Yelamanchili, and Sarah L. Lappin. Multifocal Atrial Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459152/, CC BY 4.0.",True,Text,,,,
0d21bd73-643d-41a6-990a-915a248f2b38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Farzam, Khashayar, and John R. Richards. Premature Ventricular Contraction. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532991/, CC BY 4.0.",True,Text,,,,
8f9ddae3-6aea-46b7-8d30-369f8ad6a675,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Foth, Christopher, Manesh Kumar Gangwani, and Heidi Alvey. Ventricular Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532954/, CC BY 4.0.",True,Text,,,,
7315675a-f216-4503-84dd-601b0c5bbaf2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Hafeez, Yamama, and Shamai A. Grossman. Sinus Bradycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK493201/, CC BY 4.0.",True,Text,,,,
c46fc0ea-0084-4070-a35b-0b2fbd306c7f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Harkness, Weston T., and Mary Hicks. Right Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK507872/, CC BY 4.0.",True,Text,,,,
91123750-c423-410a-98c9-51df8665fae0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Heaton, Joseph, and Srikanth Yandrapalli. Premature Atrial Contractions. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK559204/, CC BY 4.0.",True,Text,,,,
33afce11-28e0-4fb6-9ad8-9ce4511e6ad6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Kashou, Anthony H., Amandeep Goyal, Tran Nguyen, and Lovely Chhabra. Atrioventricular Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459147/, CC BY 4.0.",True,Text,,,,
4c24b859-9d3e-4088-8174-c008a3088997,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,“Learn the Heart.” Healio. https://www.healio.com/cardiology/learn-the-heart.,True,Text,,,,
aa06e937-a3a2-4364-bb24-7d0b7af5cda8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Ludhwani, Dipesh, Amandeep Goyal, and Mandar Jagtap. Ventricular Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK537120/, CC BY 4.0.",True,Text,,,,
73ed1c58-f232-4445-af64-958117caafac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Nesheiwat, Zeid, Amandeep Goyal, and Mandar Jagtap. Atrial Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK526072/, CC BY 4.0.",True,Text,,,,
3313f5ab-96e2-465f-be46-540b30c7fc5c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Pipilas, Daniel C., Bruce A. Koplan, and Leonard S. Lilly. “The Electrocardiogram.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 4. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
07bdb892-0188-4b39-a447-8eafe0dc81aa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Rodriguez Ziccardi, Mary, Amandeep Goyal, and Christopher V. Maani. Atrial Flutter. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK540985/, CC BY 4.0.",True,Text,,,,
04a409fb-0a77-4013-a83f-38a01d1c722f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-6,"Scherbak, Dmitriy, and Gregory J. Hicks. Left Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK482167/, CC BY 4.0.",True,Text,,,,
314ee30f-64f4-4b00-be1a-8e4492245efa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,USMLE,False,USMLE,,,,
f18cd2e3-4ba8-4445-82e6-f3629148134d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f18cd2e3-4ba8-4445-82e6-f3629148134d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f18cd2e3-4ba8-4445-82e6-f3629148134d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f18cd2e3-4ba8-4445-82e6-f3629148134d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f18cd2e3-4ba8-4445-82e6-f3629148134d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f18cd2e3-4ba8-4445-82e6-f3629148134d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f18cd2e3-4ba8-4445-82e6-f3629148134d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f18cd2e3-4ba8-4445-82e6-f3629148134d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f18cd2e3-4ba8-4445-82e6-f3629148134d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f18cd2e3-4ba8-4445-82e6-f3629148134d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f18cd2e3-4ba8-4445-82e6-f3629148134d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f18cd2e3-4ba8-4445-82e6-f3629148134d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f18cd2e3-4ba8-4445-82e6-f3629148134d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f18cd2e3-4ba8-4445-82e6-f3629148134d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f18cd2e3-4ba8-4445-82e6-f3629148134d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f18cd2e3-4ba8-4445-82e6-f3629148134d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f18cd2e3-4ba8-4445-82e6-f3629148134d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
96c935d8-673e-4bcb-a88c-5507fbd0ed64,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,10q22,False,10q22,,,,
d8e7317c-a8b3-4a35-a4d0-c80205b9f14a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,q24,False,q24,,,,
13c8bd9e-eddd-4dd1-b704-e27b9c4a6764,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,fibrillatory,False,fibrillatory,,,,
8a6467ab-5525-44af-b1fa-92fb863735b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8a6467ab-5525-44af-b1fa-92fb863735b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8a6467ab-5525-44af-b1fa-92fb863735b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8a6467ab-5525-44af-b1fa-92fb863735b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8a6467ab-5525-44af-b1fa-92fb863735b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8a6467ab-5525-44af-b1fa-92fb863735b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8a6467ab-5525-44af-b1fa-92fb863735b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8a6467ab-5525-44af-b1fa-92fb863735b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8a6467ab-5525-44af-b1fa-92fb863735b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8a6467ab-5525-44af-b1fa-92fb863735b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8a6467ab-5525-44af-b1fa-92fb863735b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8a6467ab-5525-44af-b1fa-92fb863735b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8a6467ab-5525-44af-b1fa-92fb863735b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8a6467ab-5525-44af-b1fa-92fb863735b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8a6467ab-5525-44af-b1fa-92fb863735b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8a6467ab-5525-44af-b1fa-92fb863735b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
8a6467ab-5525-44af-b1fa-92fb863735b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
9ecaa88c-d1ac-4d31-95d5-fdce7e4bb8f2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Table 1.1: Atrial fibrillation summary.,True,fibrillatory,,,,
7ae3b3be-38b0-4996-afd9-81c10b4fc7f2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Atrial Flutter,False,Atrial Flutter,,,,
e364dff6-96da-41cc-89c6-5db479bacf49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
e364dff6-96da-41cc-89c6-5db479bacf49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
e364dff6-96da-41cc-89c6-5db479bacf49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
e364dff6-96da-41cc-89c6-5db479bacf49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
e364dff6-96da-41cc-89c6-5db479bacf49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
e364dff6-96da-41cc-89c6-5db479bacf49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
e364dff6-96da-41cc-89c6-5db479bacf49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
e364dff6-96da-41cc-89c6-5db479bacf49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
e364dff6-96da-41cc-89c6-5db479bacf49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
e364dff6-96da-41cc-89c6-5db479bacf49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
e364dff6-96da-41cc-89c6-5db479bacf49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
e364dff6-96da-41cc-89c6-5db479bacf49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
e364dff6-96da-41cc-89c6-5db479bacf49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
e364dff6-96da-41cc-89c6-5db479bacf49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
e364dff6-96da-41cc-89c6-5db479bacf49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
e364dff6-96da-41cc-89c6-5db479bacf49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
e364dff6-96da-41cc-89c6-5db479bacf49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
240bb132-4469-4d30-a435-53580e0c626f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,macroreentrant,False,macroreentrant,,,,
7341a762-e6b2-4327-aca5-e07b338e3515,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,cavotricuspid,False,cavotricuspid,,,,
9b694ac1-cb71-44e3-b180-3a496b896f84,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"As with atrial fibrillation, the AV node’s refractory period prevents most of the P-waves from progressing to the ventricle, but commonly the AV conduction will be 2-to-1, so with an atrial rate of 300 bpm the ventricular rate will be 150 bpm. Parasympathetic stimulation or changes in AV node refractoriness can modify how many P-waves pass into the ventricle, but the the resultant rhythm is “regularly irregular.” When the heart rate is elevated, then distinguishing flutter from fibrillation becomes challenging and slowing ventricular rate pharmaceutically (adenosine) helps the flutter waves reemerge for a definitive diagnosis to be made.",True,cavotricuspid,,,,
e16c314b-7c5d-409b-81dc-12d547759e3a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Table 1.2: Atrial flutter summary.,True,cavotricuspid,,,,
953d3214-1cd8-4a29-a761-2b1450a6788b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Multifocal Atrial Tachycardia,False,Multifocal Atrial Tachycardia,,,,
435a6bb5-7e01-4277-9288-d22a7c1e0934,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
435a6bb5-7e01-4277-9288-d22a7c1e0934,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
435a6bb5-7e01-4277-9288-d22a7c1e0934,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
435a6bb5-7e01-4277-9288-d22a7c1e0934,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
435a6bb5-7e01-4277-9288-d22a7c1e0934,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
435a6bb5-7e01-4277-9288-d22a7c1e0934,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
435a6bb5-7e01-4277-9288-d22a7c1e0934,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
435a6bb5-7e01-4277-9288-d22a7c1e0934,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
435a6bb5-7e01-4277-9288-d22a7c1e0934,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
435a6bb5-7e01-4277-9288-d22a7c1e0934,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
435a6bb5-7e01-4277-9288-d22a7c1e0934,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
435a6bb5-7e01-4277-9288-d22a7c1e0934,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
435a6bb5-7e01-4277-9288-d22a7c1e0934,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
435a6bb5-7e01-4277-9288-d22a7c1e0934,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
435a6bb5-7e01-4277-9288-d22a7c1e0934,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
435a6bb5-7e01-4277-9288-d22a7c1e0934,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
435a6bb5-7e01-4277-9288-d22a7c1e0934,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
783d5cc7-cf0e-447d-a54d-b6f1f102cfa0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"MAT frequently occurs in the setting of severe lung disease and, more specifically, during an exacerbation of lung disease. This rhythm is benign, and once the underlying lung disease is treated, it should resolve.",True,Multifocal Atrial Tachycardia,,,,
8b719392-c623-4373-83d7-1dce8555bb45,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Table 1.3: MAT summary.,True,Multifocal Atrial Tachycardia,,,,
70c1f9c9-4863-47c7-b02c-ed5fefc7473f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Premature Atrial Contraction,False,Premature Atrial Contraction,,,,
43133727-2b41-4a90-bfe8-62dd191dc25a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A premature atrial contraction (PAC) is generated by a depolarization instigated outside of the SA node. This produces an extra P-wave, and consequently a shortening from previous P-P intervals is seen. The aberrant P-wave also has a different morphology from a sinus P-wave because of its different anatomical origin.",True,Premature Atrial Contraction,,,,
afbec4b0-2b14-4669-99c7-f90db97d6455,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
afbec4b0-2b14-4669-99c7-f90db97d6455,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
afbec4b0-2b14-4669-99c7-f90db97d6455,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
afbec4b0-2b14-4669-99c7-f90db97d6455,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
afbec4b0-2b14-4669-99c7-f90db97d6455,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
afbec4b0-2b14-4669-99c7-f90db97d6455,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
afbec4b0-2b14-4669-99c7-f90db97d6455,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
afbec4b0-2b14-4669-99c7-f90db97d6455,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
afbec4b0-2b14-4669-99c7-f90db97d6455,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
afbec4b0-2b14-4669-99c7-f90db97d6455,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
afbec4b0-2b14-4669-99c7-f90db97d6455,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
afbec4b0-2b14-4669-99c7-f90db97d6455,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
afbec4b0-2b14-4669-99c7-f90db97d6455,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
afbec4b0-2b14-4669-99c7-f90db97d6455,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
afbec4b0-2b14-4669-99c7-f90db97d6455,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
afbec4b0-2b14-4669-99c7-f90db97d6455,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
afbec4b0-2b14-4669-99c7-f90db97d6455,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
92751ca0-8f98-4ba5-b46e-683abc715a85,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"If a PAC occurs when the AV node has not yet recovered from its refractory period, the PAC will fail to conduct to the ventricles; meaning the PAC will not be followed by a QRS complex or the ectopic P-R interval will be prolonged. The ECG will show a premature, ectopic P-wave and then no QRS complex afterward. When this occurs along with bigeminy, the ECG can appear as if there is sinus bradycardia.",True,Premature Atrial Contraction,,,,
2a11520e-4e9f-4101-9add-4c6f5a749039,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Table 1.4: PAC summary.,True,Premature Atrial Contraction,,,,
5c39e52d-4fb4-4972-89ef-076c51d610af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Sinus Bradycardia,False,Sinus Bradycardia,,,,
dac58a3b-f597-49ff-a671-38cec8fe728f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Sinus bradycardia denotes a sinus rhythm below 60 bpm. Otherwise the ECG waveform is normal on an ECG with an upright P-wave in lead II preceding every QRS complex. There are many intrinsic causes associated with the heart itself, as well as extrinsic causes, some of which are listed table 1.5. Sinus bradycardia is usually asymptomatic as rates of 40–50 bpm can maintain hemodynamic stability. Rates below this can produce symptoms of fatigue, dizziness, and dyspnea on exertion.",True,Sinus Bradycardia,,,,
5812fe89-717b-4fea-962a-9e8c7c64a7c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Table 1.5: Intrinsic and extrinsic causes associated with the heart.,True,Sinus Bradycardia,,,,
5d7e4b1e-b5ce-40b2-809a-15aa35bb74d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Table 1.6: Sinus bradycardia summary.,True,Sinus Bradycardia,,,,
8fe10580-1c5f-461b-99ee-48e7a41d5b4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Premature Ventricular Contractions,False,Premature Ventricular Contractions,,,,
6145adea-1576-4fee-8afa-95b6f4d81770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
6145adea-1576-4fee-8afa-95b6f4d81770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
6145adea-1576-4fee-8afa-95b6f4d81770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
6145adea-1576-4fee-8afa-95b6f4d81770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
6145adea-1576-4fee-8afa-95b6f4d81770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
6145adea-1576-4fee-8afa-95b6f4d81770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
6145adea-1576-4fee-8afa-95b6f4d81770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
6145adea-1576-4fee-8afa-95b6f4d81770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
6145adea-1576-4fee-8afa-95b6f4d81770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
6145adea-1576-4fee-8afa-95b6f4d81770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
6145adea-1576-4fee-8afa-95b6f4d81770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
6145adea-1576-4fee-8afa-95b6f4d81770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
6145adea-1576-4fee-8afa-95b6f4d81770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
6145adea-1576-4fee-8afa-95b6f4d81770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
6145adea-1576-4fee-8afa-95b6f4d81770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
6145adea-1576-4fee-8afa-95b6f4d81770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
6145adea-1576-4fee-8afa-95b6f4d81770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
35059dd0-3972-4759-a39e-f7543667c230,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Table 1.7: PVC summary.,True,Premature Ventricular Contractions,,,,
12f35628-baa0-4c6a-8784-09f8b12c2569,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Ventricular Tachycardia,False,Ventricular Tachycardia,,,,
83a7165d-bcb3-4137-8ed6-59d7b0a60fc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Ventricular tachycardia (VT) is caused by reentry currents being established in the ventricular myocardium or groups of ventricular myocytes that have aberrant electrical behavior. As such, VT is usually caused by underlying cardiac disease.",True,Ventricular Tachycardia,,,,
b679416d-cce5-4829-a2a2-8d9f508440c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Like a PVC, the aberrant depolarizations do not follow the normal conduction pathways so are wide (>120 msecs), but unlike a PVC, VT involves a ventricular rate >100 bpm. With disorganized contractility and reduced filling time, VT can lead to hemodynamic instability and severe hypotension—hence it is life threatening.",True,Ventricular Tachycardia,,,,
88b4744a-6e56-4df8-ade6-d14ad43e65a1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The QRS morphology in VT is highly variable between patients and depends on where the arrhythmia originates. Consequently there are several ways to classify VT based on duration, symptoms, QRS morphology, rate, and origin.",True,Ventricular Tachycardia,,,,
c25b2a72-6a2c-417d-a0f4-98df09ceeeb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Sustained VT is any VT that lasts for more than 30 seconds or is symptomatic. Nonsustained VT lasts for less than 30 seconds and is asymptomatic.,True,Ventricular Tachycardia,,,,
f34ae5d5-448e-442d-aa9a-23de7450e288,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f34ae5d5-448e-442d-aa9a-23de7450e288,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f34ae5d5-448e-442d-aa9a-23de7450e288,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f34ae5d5-448e-442d-aa9a-23de7450e288,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f34ae5d5-448e-442d-aa9a-23de7450e288,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f34ae5d5-448e-442d-aa9a-23de7450e288,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f34ae5d5-448e-442d-aa9a-23de7450e288,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f34ae5d5-448e-442d-aa9a-23de7450e288,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f34ae5d5-448e-442d-aa9a-23de7450e288,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f34ae5d5-448e-442d-aa9a-23de7450e288,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f34ae5d5-448e-442d-aa9a-23de7450e288,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f34ae5d5-448e-442d-aa9a-23de7450e288,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f34ae5d5-448e-442d-aa9a-23de7450e288,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f34ae5d5-448e-442d-aa9a-23de7450e288,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f34ae5d5-448e-442d-aa9a-23de7450e288,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f34ae5d5-448e-442d-aa9a-23de7450e288,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f34ae5d5-448e-442d-aa9a-23de7450e288,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
8d82a4dc-96ee-4837-af09-969188bfe3d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
8d82a4dc-96ee-4837-af09-969188bfe3d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
8d82a4dc-96ee-4837-af09-969188bfe3d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
8d82a4dc-96ee-4837-af09-969188bfe3d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
8d82a4dc-96ee-4837-af09-969188bfe3d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
8d82a4dc-96ee-4837-af09-969188bfe3d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
8d82a4dc-96ee-4837-af09-969188bfe3d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
8d82a4dc-96ee-4837-af09-969188bfe3d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
8d82a4dc-96ee-4837-af09-969188bfe3d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
8d82a4dc-96ee-4837-af09-969188bfe3d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
8d82a4dc-96ee-4837-af09-969188bfe3d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
8d82a4dc-96ee-4837-af09-969188bfe3d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
8d82a4dc-96ee-4837-af09-969188bfe3d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
8d82a4dc-96ee-4837-af09-969188bfe3d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
8d82a4dc-96ee-4837-af09-969188bfe3d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
8d82a4dc-96ee-4837-af09-969188bfe3d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
8d82a4dc-96ee-4837-af09-969188bfe3d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
c93471d0-16b5-4484-93de-48da6ee3f202,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Torsades de pointes is associated with a prolonged QT interval (>600 msecs) that helps distinguish it from other forms of polymorphous VT. The longer QT interval can be caused by ionic abnormalities that reduce the repolarizing current of Phase 3 of the cardiac action potential. This makes the myocardium susceptible to early after-depolarizations—the trigger for torsades de pointes. These after-depolarizations do not happen uniformly across the myocardium and are more common in endocardial tissue where the repolarization currents are slower. So torsades de pointes arises from the after-depolarizations causing reentry currents in neighboring tissue.,True,Ventricular Tachycardia,,,,
d10758d4-7e45-4639-9101-821c98bca345,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Both common garden variety VTs and torsades de pointes can progress to ventricular fibrillation.,True,Ventricular Tachycardia,,,,
8a2d6fe2-62ab-474b-b7cb-a74586eb74c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Table 1.8: VT summary.,True,Ventricular Tachycardia,,,,
51d34251-bf73-4feb-90ed-4b98c1c34d90,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Ventricular Fibrillation,False,Ventricular Fibrillation,,,,
678db58d-ce7c-48b2-a4ef-1b866011c408,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Ventricular fibrillation (VF) occurs when the ventricular rate exceeds 400 bpm. The disorganized and uncoordinated contraction of the myocardium causes cardiac output to fall to catastrophic levels. Rates of survival for out-of-hospital VF are low.,True,Ventricular Fibrillation,,,,
da3735d6-e98d-4844-9335-02c48391eda9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
da3735d6-e98d-4844-9335-02c48391eda9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
da3735d6-e98d-4844-9335-02c48391eda9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
da3735d6-e98d-4844-9335-02c48391eda9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
da3735d6-e98d-4844-9335-02c48391eda9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
da3735d6-e98d-4844-9335-02c48391eda9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
da3735d6-e98d-4844-9335-02c48391eda9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
da3735d6-e98d-4844-9335-02c48391eda9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
da3735d6-e98d-4844-9335-02c48391eda9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
da3735d6-e98d-4844-9335-02c48391eda9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
da3735d6-e98d-4844-9335-02c48391eda9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
da3735d6-e98d-4844-9335-02c48391eda9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
da3735d6-e98d-4844-9335-02c48391eda9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
da3735d6-e98d-4844-9335-02c48391eda9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
da3735d6-e98d-4844-9335-02c48391eda9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
da3735d6-e98d-4844-9335-02c48391eda9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
da3735d6-e98d-4844-9335-02c48391eda9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
f289f1cb-260c-4eae-a47a-a6d247391573,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Table 1.9: VF summary.,True,Ventricular Fibrillation,,,,
b4dbaeed-348e-4b95-9f3c-e6c31b02b9b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,First-Degree Atrioventricular Block,False,First-Degree Atrioventricular Block,,,,
608882c5-b187-43d9-8dce-f6c269fd2575,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
608882c5-b187-43d9-8dce-f6c269fd2575,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
608882c5-b187-43d9-8dce-f6c269fd2575,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
608882c5-b187-43d9-8dce-f6c269fd2575,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
608882c5-b187-43d9-8dce-f6c269fd2575,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
608882c5-b187-43d9-8dce-f6c269fd2575,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
608882c5-b187-43d9-8dce-f6c269fd2575,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
608882c5-b187-43d9-8dce-f6c269fd2575,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
608882c5-b187-43d9-8dce-f6c269fd2575,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
608882c5-b187-43d9-8dce-f6c269fd2575,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
608882c5-b187-43d9-8dce-f6c269fd2575,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
608882c5-b187-43d9-8dce-f6c269fd2575,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
608882c5-b187-43d9-8dce-f6c269fd2575,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
608882c5-b187-43d9-8dce-f6c269fd2575,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
608882c5-b187-43d9-8dce-f6c269fd2575,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
608882c5-b187-43d9-8dce-f6c269fd2575,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
608882c5-b187-43d9-8dce-f6c269fd2575,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f5572fd3-43ae-4573-ac26-afa5d58dbe74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f5572fd3-43ae-4573-ac26-afa5d58dbe74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f5572fd3-43ae-4573-ac26-afa5d58dbe74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f5572fd3-43ae-4573-ac26-afa5d58dbe74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f5572fd3-43ae-4573-ac26-afa5d58dbe74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f5572fd3-43ae-4573-ac26-afa5d58dbe74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f5572fd3-43ae-4573-ac26-afa5d58dbe74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f5572fd3-43ae-4573-ac26-afa5d58dbe74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f5572fd3-43ae-4573-ac26-afa5d58dbe74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f5572fd3-43ae-4573-ac26-afa5d58dbe74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f5572fd3-43ae-4573-ac26-afa5d58dbe74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f5572fd3-43ae-4573-ac26-afa5d58dbe74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f5572fd3-43ae-4573-ac26-afa5d58dbe74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f5572fd3-43ae-4573-ac26-afa5d58dbe74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f5572fd3-43ae-4573-ac26-afa5d58dbe74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f5572fd3-43ae-4573-ac26-afa5d58dbe74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f5572fd3-43ae-4573-ac26-afa5d58dbe74,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
becd3195-8154-40f3-9f3b-d6c1928286fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Table 1.10: First-degree block summary.,True,First-Degree Atrioventricular Block,,,,
90ce5500-303a-4091-9930-5a547f4d36c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Second-Degree Atrioventricular Block,False,Second-Degree Atrioventricular Block,,,,
64e65360-e775-4f95-881f-d9145187f49e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A second-degree atrioventricular block also has changes in P-R interval, but it starts to show failure of the P-wave to propagate a QRS complex every time (i.e., intermittently the depolarization fails to reach the ventricles). The pattern of missed ventricular depolarizations, or blocked P-waves, is often very regular and described as a ratio of P-waves to QRS complex. The way in which the P-R interval changes in relation to the blocked P-waves produces subclassifications of second-degree blocks, Mobitz I and II.",True,Second-Degree Atrioventricular Block,,,,
41747e4d-476c-4bec-995d-8670be3a8f7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
41747e4d-476c-4bec-995d-8670be3a8f7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
41747e4d-476c-4bec-995d-8670be3a8f7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
41747e4d-476c-4bec-995d-8670be3a8f7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
41747e4d-476c-4bec-995d-8670be3a8f7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
41747e4d-476c-4bec-995d-8670be3a8f7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
41747e4d-476c-4bec-995d-8670be3a8f7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
41747e4d-476c-4bec-995d-8670be3a8f7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
41747e4d-476c-4bec-995d-8670be3a8f7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
41747e4d-476c-4bec-995d-8670be3a8f7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
41747e4d-476c-4bec-995d-8670be3a8f7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
41747e4d-476c-4bec-995d-8670be3a8f7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
41747e4d-476c-4bec-995d-8670be3a8f7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
41747e4d-476c-4bec-995d-8670be3a8f7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
41747e4d-476c-4bec-995d-8670be3a8f7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
41747e4d-476c-4bec-995d-8670be3a8f7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
41747e4d-476c-4bec-995d-8670be3a8f7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
a87956e2-eabf-4613-b0a5-ac9f7bda2ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a87956e2-eabf-4613-b0a5-ac9f7bda2ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a87956e2-eabf-4613-b0a5-ac9f7bda2ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a87956e2-eabf-4613-b0a5-ac9f7bda2ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a87956e2-eabf-4613-b0a5-ac9f7bda2ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a87956e2-eabf-4613-b0a5-ac9f7bda2ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a87956e2-eabf-4613-b0a5-ac9f7bda2ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a87956e2-eabf-4613-b0a5-ac9f7bda2ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a87956e2-eabf-4613-b0a5-ac9f7bda2ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a87956e2-eabf-4613-b0a5-ac9f7bda2ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a87956e2-eabf-4613-b0a5-ac9f7bda2ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a87956e2-eabf-4613-b0a5-ac9f7bda2ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a87956e2-eabf-4613-b0a5-ac9f7bda2ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a87956e2-eabf-4613-b0a5-ac9f7bda2ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a87956e2-eabf-4613-b0a5-ac9f7bda2ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a87956e2-eabf-4613-b0a5-ac9f7bda2ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a87956e2-eabf-4613-b0a5-ac9f7bda2ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
1c3a8fc9-6670-4914-8406-5a831f7f6dae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Table 1.11: Second-degree block summary.,True,Second-Degree Atrioventricular Block,,,,
a06839a6-c0d8-49ab-977f-2cb35c30db8e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Third-Degree Atrioventricular Block,False,Third-Degree Atrioventricular Block,,,,
b5ce088f-9a71-4b62-bc67-f133fd1e72a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b5ce088f-9a71-4b62-bc67-f133fd1e72a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b5ce088f-9a71-4b62-bc67-f133fd1e72a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b5ce088f-9a71-4b62-bc67-f133fd1e72a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b5ce088f-9a71-4b62-bc67-f133fd1e72a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b5ce088f-9a71-4b62-bc67-f133fd1e72a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b5ce088f-9a71-4b62-bc67-f133fd1e72a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b5ce088f-9a71-4b62-bc67-f133fd1e72a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b5ce088f-9a71-4b62-bc67-f133fd1e72a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b5ce088f-9a71-4b62-bc67-f133fd1e72a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b5ce088f-9a71-4b62-bc67-f133fd1e72a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b5ce088f-9a71-4b62-bc67-f133fd1e72a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b5ce088f-9a71-4b62-bc67-f133fd1e72a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b5ce088f-9a71-4b62-bc67-f133fd1e72a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b5ce088f-9a71-4b62-bc67-f133fd1e72a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b5ce088f-9a71-4b62-bc67-f133fd1e72a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b5ce088f-9a71-4b62-bc67-f133fd1e72a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
9e098eda-b964-4a05-8f4b-558925f09129,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Table 1.12: Third-degree block summary.,True,Third-Degree Atrioventricular Block,,,,
66a7fbe1-7690-4119-9dc6-a8e8049ccac1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Left Bundle Branch Block,False,Left Bundle Branch Block,,,,
f3588c38-248e-4cf5-a596-4abc549ff37a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"A left bundle branch block (LBBB) is generated when the conductivity of the His-Purkinje system in the left ventricle is compromised, either through damage or disease. The ECG changes, and criteria for LBBB relate to these changes in conductivity and the left-side location.",True,Left Bundle Branch Block,,,,
253d41f1-19cf-4c5b-82d8-06d9a4197f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
253d41f1-19cf-4c5b-82d8-06d9a4197f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
253d41f1-19cf-4c5b-82d8-06d9a4197f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
253d41f1-19cf-4c5b-82d8-06d9a4197f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
253d41f1-19cf-4c5b-82d8-06d9a4197f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
253d41f1-19cf-4c5b-82d8-06d9a4197f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
253d41f1-19cf-4c5b-82d8-06d9a4197f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
253d41f1-19cf-4c5b-82d8-06d9a4197f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
253d41f1-19cf-4c5b-82d8-06d9a4197f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
253d41f1-19cf-4c5b-82d8-06d9a4197f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
253d41f1-19cf-4c5b-82d8-06d9a4197f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
253d41f1-19cf-4c5b-82d8-06d9a4197f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
253d41f1-19cf-4c5b-82d8-06d9a4197f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
253d41f1-19cf-4c5b-82d8-06d9a4197f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
253d41f1-19cf-4c5b-82d8-06d9a4197f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
253d41f1-19cf-4c5b-82d8-06d9a4197f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
253d41f1-19cf-4c5b-82d8-06d9a4197f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
4c328aa0-9890-4221-a0b9-1bce4dcc585b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The lateral leads (I, V5, and V6) normally show a downward deflecting Q-wave as normal septal deflection initially occurs left-to-right (i.e., away from the lateral leads). In LBBB the change in direction to right-to-left, plus the longer duration, eliminates the Q-wave from the lateral leads, and Q-waves will be small in aVL.",True,Left Bundle Branch Block,,,,
eb0d85d0-f9aa-419c-b744-df6d8f9291ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
eb0d85d0-f9aa-419c-b744-df6d8f9291ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
eb0d85d0-f9aa-419c-b744-df6d8f9291ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
eb0d85d0-f9aa-419c-b744-df6d8f9291ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
eb0d85d0-f9aa-419c-b744-df6d8f9291ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
eb0d85d0-f9aa-419c-b744-df6d8f9291ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
eb0d85d0-f9aa-419c-b744-df6d8f9291ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
eb0d85d0-f9aa-419c-b744-df6d8f9291ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
eb0d85d0-f9aa-419c-b744-df6d8f9291ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
eb0d85d0-f9aa-419c-b744-df6d8f9291ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
eb0d85d0-f9aa-419c-b744-df6d8f9291ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
eb0d85d0-f9aa-419c-b744-df6d8f9291ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
eb0d85d0-f9aa-419c-b744-df6d8f9291ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
eb0d85d0-f9aa-419c-b744-df6d8f9291ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
eb0d85d0-f9aa-419c-b744-df6d8f9291ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
eb0d85d0-f9aa-419c-b744-df6d8f9291ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
eb0d85d0-f9aa-419c-b744-df6d8f9291ca,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
b02d90be-e946-4463-bbb3-ba653704acda,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b02d90be-e946-4463-bbb3-ba653704acda,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b02d90be-e946-4463-bbb3-ba653704acda,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b02d90be-e946-4463-bbb3-ba653704acda,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b02d90be-e946-4463-bbb3-ba653704acda,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b02d90be-e946-4463-bbb3-ba653704acda,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b02d90be-e946-4463-bbb3-ba653704acda,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b02d90be-e946-4463-bbb3-ba653704acda,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b02d90be-e946-4463-bbb3-ba653704acda,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b02d90be-e946-4463-bbb3-ba653704acda,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b02d90be-e946-4463-bbb3-ba653704acda,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b02d90be-e946-4463-bbb3-ba653704acda,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b02d90be-e946-4463-bbb3-ba653704acda,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b02d90be-e946-4463-bbb3-ba653704acda,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b02d90be-e946-4463-bbb3-ba653704acda,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b02d90be-e946-4463-bbb3-ba653704acda,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b02d90be-e946-4463-bbb3-ba653704acda,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
16189f19-8908-4e86-ab9a-32e17472b576,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Table 1.13: LBBB summary.,True,Left Bundle Branch Block,,,,
5db979ec-105e-48e7-ad42-2b8858c80da4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Right Bundle Branch Block,False,Right Bundle Branch Block,,,,
a95fac4f-c458-4a9f-a0de-2641127c6124,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The causes and manifestations of a right bundle branch block (RBBB) bear some similarities to those described for LBBB, but of course this time its depolarization of the right ventricle is delayed. Causes of RBBB include ischemic heart disease again as well as other myocardial diseases, but pulmonary issues such as pulmonary embolism and cor pulmonale can be added to the list.",True,Right Bundle Branch Block,,,,
ffd78231-0c62-49ef-9bd0-3723a3a82aec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
ffd78231-0c62-49ef-9bd0-3723a3a82aec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
ffd78231-0c62-49ef-9bd0-3723a3a82aec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
ffd78231-0c62-49ef-9bd0-3723a3a82aec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
ffd78231-0c62-49ef-9bd0-3723a3a82aec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
ffd78231-0c62-49ef-9bd0-3723a3a82aec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
ffd78231-0c62-49ef-9bd0-3723a3a82aec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
ffd78231-0c62-49ef-9bd0-3723a3a82aec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
ffd78231-0c62-49ef-9bd0-3723a3a82aec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
ffd78231-0c62-49ef-9bd0-3723a3a82aec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
ffd78231-0c62-49ef-9bd0-3723a3a82aec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
ffd78231-0c62-49ef-9bd0-3723a3a82aec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
ffd78231-0c62-49ef-9bd0-3723a3a82aec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
ffd78231-0c62-49ef-9bd0-3723a3a82aec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
ffd78231-0c62-49ef-9bd0-3723a3a82aec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
ffd78231-0c62-49ef-9bd0-3723a3a82aec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
ffd78231-0c62-49ef-9bd0-3723a3a82aec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
59936d70-e6e9-46b6-b5da-3e76d34e91ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Table 1.14: RBBB summary.,True,Right Bundle Branch Block,,,,
5491d8a0-d1b5-443e-871c-53fbbfa989ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Wolff-Parkinson-White Syndrome,False,Wolff-Parkinson-White Syndrome,,,,
2a235fd8-b09a-4a29-8dcc-6e61b86ff09b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Normally the only electrical connection between the atria and the ventricles is the AV node. Otherwise the fibrous skeleton of the heart electrically insulates the atria from the ventricles. In Wolff-Parkinson-White (WPW) syndrome, that insulation is incomplete, and an “accessory pathway” connects the electrical system of the atria directly to the ventricles. If you think of the AV node as a bridge over the fibrous wall with regulated access, the accessory pathway is like a pathological tunnel under it with no regulation.",True,Wolff-Parkinson-White Syndrome,,,,
40d9daf5-b340-4ff4-9e9b-4ee65c04e627,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
40d9daf5-b340-4ff4-9e9b-4ee65c04e627,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
40d9daf5-b340-4ff4-9e9b-4ee65c04e627,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
40d9daf5-b340-4ff4-9e9b-4ee65c04e627,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
40d9daf5-b340-4ff4-9e9b-4ee65c04e627,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
40d9daf5-b340-4ff4-9e9b-4ee65c04e627,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
40d9daf5-b340-4ff4-9e9b-4ee65c04e627,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
40d9daf5-b340-4ff4-9e9b-4ee65c04e627,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
40d9daf5-b340-4ff4-9e9b-4ee65c04e627,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
40d9daf5-b340-4ff4-9e9b-4ee65c04e627,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
40d9daf5-b340-4ff4-9e9b-4ee65c04e627,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
40d9daf5-b340-4ff4-9e9b-4ee65c04e627,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
40d9daf5-b340-4ff4-9e9b-4ee65c04e627,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
40d9daf5-b340-4ff4-9e9b-4ee65c04e627,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
40d9daf5-b340-4ff4-9e9b-4ee65c04e627,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
40d9daf5-b340-4ff4-9e9b-4ee65c04e627,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
40d9daf5-b340-4ff4-9e9b-4ee65c04e627,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
1b4c16f4-32ee-4ef1-b75a-61f5e0c60a40,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"WPW syndrome is often asymptomatic, and patients do not require immediate treatment. However, if atrial fibrillation occurs in a WPW patient, the accessory pathway can allow the atrial fibrillation waves through to the ventricle (with no AV nodal refractory period to prevent them). Consequently a high ventricular rate is seen, and the risk of ventricular fibrillation being established means immediate clinical attention is required.",True,Wolff-Parkinson-White Syndrome,,,,
04b06ba0-77ad-4f87-b313-161d32ace14a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Hyper- and Hypocalcemia,False,Hyper- and Hypocalcemia,,,,
3b2cf5fd-21ee-4460-b6a8-ecfec96814e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3b2cf5fd-21ee-4460-b6a8-ecfec96814e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3b2cf5fd-21ee-4460-b6a8-ecfec96814e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3b2cf5fd-21ee-4460-b6a8-ecfec96814e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3b2cf5fd-21ee-4460-b6a8-ecfec96814e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3b2cf5fd-21ee-4460-b6a8-ecfec96814e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3b2cf5fd-21ee-4460-b6a8-ecfec96814e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3b2cf5fd-21ee-4460-b6a8-ecfec96814e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3b2cf5fd-21ee-4460-b6a8-ecfec96814e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3b2cf5fd-21ee-4460-b6a8-ecfec96814e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3b2cf5fd-21ee-4460-b6a8-ecfec96814e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3b2cf5fd-21ee-4460-b6a8-ecfec96814e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3b2cf5fd-21ee-4460-b6a8-ecfec96814e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3b2cf5fd-21ee-4460-b6a8-ecfec96814e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3b2cf5fd-21ee-4460-b6a8-ecfec96814e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3b2cf5fd-21ee-4460-b6a8-ecfec96814e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
3b2cf5fd-21ee-4460-b6a8-ecfec96814e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
1acb6c3b-dca8-4817-a3cc-2869c9cd7563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
1acb6c3b-dca8-4817-a3cc-2869c9cd7563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
1acb6c3b-dca8-4817-a3cc-2869c9cd7563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
1acb6c3b-dca8-4817-a3cc-2869c9cd7563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
1acb6c3b-dca8-4817-a3cc-2869c9cd7563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
1acb6c3b-dca8-4817-a3cc-2869c9cd7563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
1acb6c3b-dca8-4817-a3cc-2869c9cd7563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
1acb6c3b-dca8-4817-a3cc-2869c9cd7563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
1acb6c3b-dca8-4817-a3cc-2869c9cd7563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
1acb6c3b-dca8-4817-a3cc-2869c9cd7563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
1acb6c3b-dca8-4817-a3cc-2869c9cd7563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
1acb6c3b-dca8-4817-a3cc-2869c9cd7563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
1acb6c3b-dca8-4817-a3cc-2869c9cd7563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
1acb6c3b-dca8-4817-a3cc-2869c9cd7563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
1acb6c3b-dca8-4817-a3cc-2869c9cd7563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
1acb6c3b-dca8-4817-a3cc-2869c9cd7563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
1acb6c3b-dca8-4817-a3cc-2869c9cd7563,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
c2469923-7854-46e8-9c8c-f7fed763280a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Table 1.16: Hyper- and hypocalcemia summary.,True,Hyper- and Hypocalcemia,,,,
6979fb0f-4c16-4fa6-bb79-ef81ad003367,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Hyper- and Hypokalemia,False,Hyper- and Hypokalemia,,,,
2d827621-0043-41df-84f5-0825261fc6af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"The pathophysiology is not as simple as changes in extracellular K+ changing the electrochemical gradient for K+. Because of potassium’s role in maintaining the resting membrane potential, shifts in extracellular potassium can also influence the activity of Na+ and Ca++ channels.",True,Hyper- and Hypokalemia,,,,
acb1c2b3-820e-4424-9f61-1a51c92ddbb2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
acb1c2b3-820e-4424-9f61-1a51c92ddbb2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
acb1c2b3-820e-4424-9f61-1a51c92ddbb2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
acb1c2b3-820e-4424-9f61-1a51c92ddbb2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
acb1c2b3-820e-4424-9f61-1a51c92ddbb2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
acb1c2b3-820e-4424-9f61-1a51c92ddbb2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
acb1c2b3-820e-4424-9f61-1a51c92ddbb2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
acb1c2b3-820e-4424-9f61-1a51c92ddbb2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
acb1c2b3-820e-4424-9f61-1a51c92ddbb2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
acb1c2b3-820e-4424-9f61-1a51c92ddbb2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
acb1c2b3-820e-4424-9f61-1a51c92ddbb2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
acb1c2b3-820e-4424-9f61-1a51c92ddbb2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
acb1c2b3-820e-4424-9f61-1a51c92ddbb2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
acb1c2b3-820e-4424-9f61-1a51c92ddbb2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
acb1c2b3-820e-4424-9f61-1a51c92ddbb2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
acb1c2b3-820e-4424-9f61-1a51c92ddbb2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
acb1c2b3-820e-4424-9f61-1a51c92ddbb2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ce990c78-dc96-4e73-8a66-686857eba8c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"As hypokalemia also inhibits Na+-K+ ATPase, Na+ accumulates inside the cell. This in turn leads to an accumulation of Ca++ because of a subsequent failure of the Na+-Ca++ exchanger. Extended presence of these two positive ions inside the myocyte prolongs the action potential and may manifest as an increased width and amplitude of the P-wave.",True,Hyper- and Hypokalemia,,,,
de9c4f19-067c-4d9a-93f8-d2c84e3ab750,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"As hypokalemia worsens, the problems with K+ conductance and repolarization increase, and the myocardium becomes susceptible to early after-depolarization (EAD) arrhythmias.",True,Hyper- and Hypokalemia,,,,
8ae53c2c-f44b-4c55-be42-040f3fc8015b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
8ae53c2c-f44b-4c55-be42-040f3fc8015b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
8ae53c2c-f44b-4c55-be42-040f3fc8015b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
8ae53c2c-f44b-4c55-be42-040f3fc8015b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
8ae53c2c-f44b-4c55-be42-040f3fc8015b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
8ae53c2c-f44b-4c55-be42-040f3fc8015b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
8ae53c2c-f44b-4c55-be42-040f3fc8015b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
8ae53c2c-f44b-4c55-be42-040f3fc8015b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
8ae53c2c-f44b-4c55-be42-040f3fc8015b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
8ae53c2c-f44b-4c55-be42-040f3fc8015b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
8ae53c2c-f44b-4c55-be42-040f3fc8015b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
8ae53c2c-f44b-4c55-be42-040f3fc8015b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
8ae53c2c-f44b-4c55-be42-040f3fc8015b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
8ae53c2c-f44b-4c55-be42-040f3fc8015b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
8ae53c2c-f44b-4c55-be42-040f3fc8015b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
8ae53c2c-f44b-4c55-be42-040f3fc8015b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
8ae53c2c-f44b-4c55-be42-040f3fc8015b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
47738bbc-e463-441e-bc35-9916340a73f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
47738bbc-e463-441e-bc35-9916340a73f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
47738bbc-e463-441e-bc35-9916340a73f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
47738bbc-e463-441e-bc35-9916340a73f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
47738bbc-e463-441e-bc35-9916340a73f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
47738bbc-e463-441e-bc35-9916340a73f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
47738bbc-e463-441e-bc35-9916340a73f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
47738bbc-e463-441e-bc35-9916340a73f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
47738bbc-e463-441e-bc35-9916340a73f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
47738bbc-e463-441e-bc35-9916340a73f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
47738bbc-e463-441e-bc35-9916340a73f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
47738bbc-e463-441e-bc35-9916340a73f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
47738bbc-e463-441e-bc35-9916340a73f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
47738bbc-e463-441e-bc35-9916340a73f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
47738bbc-e463-441e-bc35-9916340a73f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
47738bbc-e463-441e-bc35-9916340a73f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
47738bbc-e463-441e-bc35-9916340a73f0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
81126493-1b94-4535-be39-24ec47e27ff5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
81126493-1b94-4535-be39-24ec47e27ff5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
81126493-1b94-4535-be39-24ec47e27ff5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
81126493-1b94-4535-be39-24ec47e27ff5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
81126493-1b94-4535-be39-24ec47e27ff5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
81126493-1b94-4535-be39-24ec47e27ff5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
81126493-1b94-4535-be39-24ec47e27ff5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
81126493-1b94-4535-be39-24ec47e27ff5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
81126493-1b94-4535-be39-24ec47e27ff5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
81126493-1b94-4535-be39-24ec47e27ff5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
81126493-1b94-4535-be39-24ec47e27ff5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
81126493-1b94-4535-be39-24ec47e27ff5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
81126493-1b94-4535-be39-24ec47e27ff5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
81126493-1b94-4535-be39-24ec47e27ff5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
81126493-1b94-4535-be39-24ec47e27ff5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
81126493-1b94-4535-be39-24ec47e27ff5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
81126493-1b94-4535-be39-24ec47e27ff5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
120cf2d6-ba0f-4047-bdb3-add6d0e785cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
120cf2d6-ba0f-4047-bdb3-add6d0e785cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
120cf2d6-ba0f-4047-bdb3-add6d0e785cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
120cf2d6-ba0f-4047-bdb3-add6d0e785cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
120cf2d6-ba0f-4047-bdb3-add6d0e785cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
120cf2d6-ba0f-4047-bdb3-add6d0e785cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
120cf2d6-ba0f-4047-bdb3-add6d0e785cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
120cf2d6-ba0f-4047-bdb3-add6d0e785cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
120cf2d6-ba0f-4047-bdb3-add6d0e785cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
120cf2d6-ba0f-4047-bdb3-add6d0e785cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
120cf2d6-ba0f-4047-bdb3-add6d0e785cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
120cf2d6-ba0f-4047-bdb3-add6d0e785cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
120cf2d6-ba0f-4047-bdb3-add6d0e785cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
120cf2d6-ba0f-4047-bdb3-add6d0e785cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
120cf2d6-ba0f-4047-bdb3-add6d0e785cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
120cf2d6-ba0f-4047-bdb3-add6d0e785cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
120cf2d6-ba0f-4047-bdb3-add6d0e785cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
5eeaa3df-1f98-4c19-abce-874faa7751c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Table 1.17: Hypo- and hyperkalemia summary.,True,Hyper- and Hypokalemia,,,,
292c35fa-47c6-4425-9a2b-2b9c49414e03,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"References, resources, and further reading",False,"References, resources, and further reading",,,,
2e083426-b134-4ea7-b02f-e26c9a7e2da7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,Text,False,Text,,,,
569a3489-93ed-4a53-97fa-e4b11ff75509,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Burns, Ed, and Robert Buttner. Hypercalcaemia. Lift in the Fast Lane, 2021. https://litfl.com/hypercalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
8eaf35f2-76ee-4bdd-8043-6c1e1ea23b0d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Burns, Ed, and Robert Buttner. Hypocalcaemia. Life in the Fast Lane, 2021. https://litfl.com/hypocalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
54089bd1-2c80-4487-b942-2668310712e9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Buttner, Robert, and Ed Burns. Hyperkalaemia. Life in the Fast Lane. https://litfl.com/hyperkalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
66f3769b-8abf-433f-af4d-4d9194ffb265,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Buttner, Robert, and Ed Burns. Hypokalaemia. Life in the Fast Lane, 2021. https://litfl.com/hypokalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
8d629c5d-2e04-456b-91f6-cb47b1d5b94f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Chhabra, Lovely, Amandeep Goyal, and Michael D. Benham. Wolff Parkinson White Syndrome. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK554437/, CC BY 4.0.",True,Text,,,,
15cf8a84-85b3-4be5-880a-31a74bbfa9b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Custer, Adam M., Varun S. Yelamanchili, and Sarah L. Lappin. Multifocal Atrial Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459152/, CC BY 4.0.",True,Text,,,,
95baeb3b-1640-4827-9ced-1ce5248fd596,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Farzam, Khashayar, and John R. Richards. Premature Ventricular Contraction. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532991/, CC BY 4.0.",True,Text,,,,
d41f3a9d-c016-4b01-877f-0525f3913b16,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Foth, Christopher, Manesh Kumar Gangwani, and Heidi Alvey. Ventricular Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532954/, CC BY 4.0.",True,Text,,,,
0232f3f7-25e8-48e8-871c-56cfbea2edf6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Hafeez, Yamama, and Shamai A. Grossman. Sinus Bradycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK493201/, CC BY 4.0.",True,Text,,,,
e52d783b-cddf-4d77-8e05-964d31276ff1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Harkness, Weston T., and Mary Hicks. Right Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK507872/, CC BY 4.0.",True,Text,,,,
d681e50e-f4b8-4dc0-879f-a5df8fe1a31b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Heaton, Joseph, and Srikanth Yandrapalli. Premature Atrial Contractions. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK559204/, CC BY 4.0.",True,Text,,,,
e4535342-01bf-4458-b584-de484bcf1615,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Kashou, Anthony H., Amandeep Goyal, Tran Nguyen, and Lovely Chhabra. Atrioventricular Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459147/, CC BY 4.0.",True,Text,,,,
922fafd2-9753-44b1-8e76-19ee088e47fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,“Learn the Heart.” Healio. https://www.healio.com/cardiology/learn-the-heart.,True,Text,,,,
e254b2ac-48a5-43dc-95b7-e23ec8306f5b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Ludhwani, Dipesh, Amandeep Goyal, and Mandar Jagtap. Ventricular Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK537120/, CC BY 4.0.",True,Text,,,,
b8f0a882-43c1-4ec6-97ee-bbeb3651217e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Nesheiwat, Zeid, Amandeep Goyal, and Mandar Jagtap. Atrial Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK526072/, CC BY 4.0.",True,Text,,,,
d014fbec-ad1c-4e03-bf53-40960eca41a6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Pipilas, Daniel C., Bruce A. Koplan, and Leonard S. Lilly. “The Electrocardiogram.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 4. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
38e59f83-4737-45e9-881e-2634a7d92606,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Rodriguez Ziccardi, Mary, Amandeep Goyal, and Christopher V. Maani. Atrial Flutter. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK540985/, CC BY 4.0.",True,Text,,,,
dc4d222d-8fdb-4ff0-b6b1-dba2c7a88cfb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Sinus Bradycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-5,"Scherbak, Dmitriy, and Gregory J. Hicks. Left Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK482167/, CC BY 4.0.",True,Text,,,,
87fa398e-f782-4c78-b6d3-7589b1ceae41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,USMLE,False,USMLE,,,,
1265c360-11c8-4ccf-88b0-a3447992834c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
1265c360-11c8-4ccf-88b0-a3447992834c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
1265c360-11c8-4ccf-88b0-a3447992834c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
1265c360-11c8-4ccf-88b0-a3447992834c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
1265c360-11c8-4ccf-88b0-a3447992834c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
1265c360-11c8-4ccf-88b0-a3447992834c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
1265c360-11c8-4ccf-88b0-a3447992834c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
1265c360-11c8-4ccf-88b0-a3447992834c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
1265c360-11c8-4ccf-88b0-a3447992834c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
1265c360-11c8-4ccf-88b0-a3447992834c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
1265c360-11c8-4ccf-88b0-a3447992834c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
1265c360-11c8-4ccf-88b0-a3447992834c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
1265c360-11c8-4ccf-88b0-a3447992834c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
1265c360-11c8-4ccf-88b0-a3447992834c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
1265c360-11c8-4ccf-88b0-a3447992834c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
1265c360-11c8-4ccf-88b0-a3447992834c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
1265c360-11c8-4ccf-88b0-a3447992834c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
d77e32a1-4e9b-46cb-8945-cd7958224960,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,10q22,False,10q22,,,,
1459107b-2dd1-43c5-8555-9a0b75dcee1b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,q24,False,q24,,,,
60a600e3-4471-4972-a767-1fe7611162a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,fibrillatory,False,fibrillatory,,,,
4eb54ed5-05f8-44c1-8b56-b0b8d699c047,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
4eb54ed5-05f8-44c1-8b56-b0b8d699c047,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
4eb54ed5-05f8-44c1-8b56-b0b8d699c047,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
4eb54ed5-05f8-44c1-8b56-b0b8d699c047,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
4eb54ed5-05f8-44c1-8b56-b0b8d699c047,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
4eb54ed5-05f8-44c1-8b56-b0b8d699c047,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
4eb54ed5-05f8-44c1-8b56-b0b8d699c047,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
4eb54ed5-05f8-44c1-8b56-b0b8d699c047,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
4eb54ed5-05f8-44c1-8b56-b0b8d699c047,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
4eb54ed5-05f8-44c1-8b56-b0b8d699c047,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
4eb54ed5-05f8-44c1-8b56-b0b8d699c047,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
4eb54ed5-05f8-44c1-8b56-b0b8d699c047,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
4eb54ed5-05f8-44c1-8b56-b0b8d699c047,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
4eb54ed5-05f8-44c1-8b56-b0b8d699c047,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
4eb54ed5-05f8-44c1-8b56-b0b8d699c047,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
4eb54ed5-05f8-44c1-8b56-b0b8d699c047,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
4eb54ed5-05f8-44c1-8b56-b0b8d699c047,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
3446fbab-e763-4658-be13-4f7a90b6715c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Table 1.1: Atrial fibrillation summary.,True,fibrillatory,,,,
a5b8c604-94af-482b-88a9-3329bdad2d4f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Atrial Flutter,False,Atrial Flutter,,,,
061ed14f-08ec-4786-95c8-6893dde8f3ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
061ed14f-08ec-4786-95c8-6893dde8f3ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
061ed14f-08ec-4786-95c8-6893dde8f3ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
061ed14f-08ec-4786-95c8-6893dde8f3ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
061ed14f-08ec-4786-95c8-6893dde8f3ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
061ed14f-08ec-4786-95c8-6893dde8f3ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
061ed14f-08ec-4786-95c8-6893dde8f3ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
061ed14f-08ec-4786-95c8-6893dde8f3ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
061ed14f-08ec-4786-95c8-6893dde8f3ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
061ed14f-08ec-4786-95c8-6893dde8f3ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
061ed14f-08ec-4786-95c8-6893dde8f3ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
061ed14f-08ec-4786-95c8-6893dde8f3ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
061ed14f-08ec-4786-95c8-6893dde8f3ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
061ed14f-08ec-4786-95c8-6893dde8f3ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
061ed14f-08ec-4786-95c8-6893dde8f3ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
061ed14f-08ec-4786-95c8-6893dde8f3ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
061ed14f-08ec-4786-95c8-6893dde8f3ae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
60450f68-b69f-4772-8b99-6f73b6567cc3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,macroreentrant,False,macroreentrant,,,,
fbfe30bc-5aeb-4ba0-be1a-879b743d0087,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,cavotricuspid,False,cavotricuspid,,,,
cacd78a8-6ee2-45de-91ab-7ff87c357d01,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"As with atrial fibrillation, the AV node’s refractory period prevents most of the P-waves from progressing to the ventricle, but commonly the AV conduction will be 2-to-1, so with an atrial rate of 300 bpm the ventricular rate will be 150 bpm. Parasympathetic stimulation or changes in AV node refractoriness can modify how many P-waves pass into the ventricle, but the the resultant rhythm is “regularly irregular.” When the heart rate is elevated, then distinguishing flutter from fibrillation becomes challenging and slowing ventricular rate pharmaceutically (adenosine) helps the flutter waves reemerge for a definitive diagnosis to be made.",True,cavotricuspid,,,,
d24044c0-ebb3-4126-9e6f-b01429992bab,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Table 1.2: Atrial flutter summary.,True,cavotricuspid,,,,
331cffbc-90c4-41e5-a7ef-233bb4223685,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Multifocal Atrial Tachycardia,False,Multifocal Atrial Tachycardia,,,,
4cde7bff-3592-4239-9d4f-16f1c29e1a2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
4cde7bff-3592-4239-9d4f-16f1c29e1a2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
4cde7bff-3592-4239-9d4f-16f1c29e1a2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
4cde7bff-3592-4239-9d4f-16f1c29e1a2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
4cde7bff-3592-4239-9d4f-16f1c29e1a2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
4cde7bff-3592-4239-9d4f-16f1c29e1a2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
4cde7bff-3592-4239-9d4f-16f1c29e1a2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
4cde7bff-3592-4239-9d4f-16f1c29e1a2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
4cde7bff-3592-4239-9d4f-16f1c29e1a2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
4cde7bff-3592-4239-9d4f-16f1c29e1a2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
4cde7bff-3592-4239-9d4f-16f1c29e1a2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
4cde7bff-3592-4239-9d4f-16f1c29e1a2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
4cde7bff-3592-4239-9d4f-16f1c29e1a2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
4cde7bff-3592-4239-9d4f-16f1c29e1a2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
4cde7bff-3592-4239-9d4f-16f1c29e1a2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
4cde7bff-3592-4239-9d4f-16f1c29e1a2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
4cde7bff-3592-4239-9d4f-16f1c29e1a2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
44e5d53b-53fe-4584-92e8-f74645240854,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"MAT frequently occurs in the setting of severe lung disease and, more specifically, during an exacerbation of lung disease. This rhythm is benign, and once the underlying lung disease is treated, it should resolve.",True,Multifocal Atrial Tachycardia,,,,
0d4c72ee-c3cd-40c9-9465-1eac1dadfea1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Table 1.3: MAT summary.,True,Multifocal Atrial Tachycardia,,,,
099ad89a-3e11-4081-b64c-9a3dcd8d66a0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Premature Atrial Contraction,False,Premature Atrial Contraction,,,,
eed61397-ca06-4033-9fb9-b813f6eb4ccc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A premature atrial contraction (PAC) is generated by a depolarization instigated outside of the SA node. This produces an extra P-wave, and consequently a shortening from previous P-P intervals is seen. The aberrant P-wave also has a different morphology from a sinus P-wave because of its different anatomical origin.",True,Premature Atrial Contraction,,,,
11b277e3-d97b-4dbb-aa2d-a66602a97a96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
11b277e3-d97b-4dbb-aa2d-a66602a97a96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
11b277e3-d97b-4dbb-aa2d-a66602a97a96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
11b277e3-d97b-4dbb-aa2d-a66602a97a96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
11b277e3-d97b-4dbb-aa2d-a66602a97a96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
11b277e3-d97b-4dbb-aa2d-a66602a97a96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
11b277e3-d97b-4dbb-aa2d-a66602a97a96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
11b277e3-d97b-4dbb-aa2d-a66602a97a96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
11b277e3-d97b-4dbb-aa2d-a66602a97a96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
11b277e3-d97b-4dbb-aa2d-a66602a97a96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
11b277e3-d97b-4dbb-aa2d-a66602a97a96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
11b277e3-d97b-4dbb-aa2d-a66602a97a96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
11b277e3-d97b-4dbb-aa2d-a66602a97a96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
11b277e3-d97b-4dbb-aa2d-a66602a97a96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
11b277e3-d97b-4dbb-aa2d-a66602a97a96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
11b277e3-d97b-4dbb-aa2d-a66602a97a96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
11b277e3-d97b-4dbb-aa2d-a66602a97a96,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
1a2953f6-29ec-4e40-8fb6-e90d8184a5b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"If a PAC occurs when the AV node has not yet recovered from its refractory period, the PAC will fail to conduct to the ventricles; meaning the PAC will not be followed by a QRS complex or the ectopic P-R interval will be prolonged. The ECG will show a premature, ectopic P-wave and then no QRS complex afterward. When this occurs along with bigeminy, the ECG can appear as if there is sinus bradycardia.",True,Premature Atrial Contraction,,,,
38780d77-a5d6-4d61-9416-1ddd07eb9906,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Table 1.4: PAC summary.,True,Premature Atrial Contraction,,,,
835585df-6c8a-4d5f-a8ee-45bb33e434bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Sinus Bradycardia,False,Sinus Bradycardia,,,,
51d56ae1-eb7e-412f-bd84-f9740586272a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Sinus bradycardia denotes a sinus rhythm below 60 bpm. Otherwise the ECG waveform is normal on an ECG with an upright P-wave in lead II preceding every QRS complex. There are many intrinsic causes associated with the heart itself, as well as extrinsic causes, some of which are listed table 1.5. Sinus bradycardia is usually asymptomatic as rates of 40–50 bpm can maintain hemodynamic stability. Rates below this can produce symptoms of fatigue, dizziness, and dyspnea on exertion.",True,Sinus Bradycardia,,,,
7f82bce4-8791-4f15-945c-cc4c4fb8c8af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Table 1.5: Intrinsic and extrinsic causes associated with the heart.,True,Sinus Bradycardia,,,,
d1422b41-8416-40c7-a011-0ce2d008f546,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Table 1.6: Sinus bradycardia summary.,True,Sinus Bradycardia,,,,
85ac79c3-8099-4ac4-93e8-b3003025c3db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Premature Ventricular Contractions,False,Premature Ventricular Contractions,,,,
3aae5fa0-009e-4dbf-bd5c-2c6f0f96e4c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3aae5fa0-009e-4dbf-bd5c-2c6f0f96e4c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3aae5fa0-009e-4dbf-bd5c-2c6f0f96e4c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3aae5fa0-009e-4dbf-bd5c-2c6f0f96e4c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3aae5fa0-009e-4dbf-bd5c-2c6f0f96e4c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3aae5fa0-009e-4dbf-bd5c-2c6f0f96e4c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3aae5fa0-009e-4dbf-bd5c-2c6f0f96e4c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3aae5fa0-009e-4dbf-bd5c-2c6f0f96e4c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3aae5fa0-009e-4dbf-bd5c-2c6f0f96e4c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3aae5fa0-009e-4dbf-bd5c-2c6f0f96e4c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3aae5fa0-009e-4dbf-bd5c-2c6f0f96e4c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3aae5fa0-009e-4dbf-bd5c-2c6f0f96e4c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3aae5fa0-009e-4dbf-bd5c-2c6f0f96e4c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3aae5fa0-009e-4dbf-bd5c-2c6f0f96e4c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3aae5fa0-009e-4dbf-bd5c-2c6f0f96e4c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3aae5fa0-009e-4dbf-bd5c-2c6f0f96e4c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3aae5fa0-009e-4dbf-bd5c-2c6f0f96e4c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
2d5a81e9-2ab9-4581-995d-d541c90bf2f3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Table 1.7: PVC summary.,True,Premature Ventricular Contractions,,,,
5c4ce832-ebc4-4ce7-83ec-7d2894a18d5c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Ventricular Tachycardia,False,Ventricular Tachycardia,,,,
c5d79ac4-459d-4f37-9f30-b06539d64f65,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Ventricular tachycardia (VT) is caused by reentry currents being established in the ventricular myocardium or groups of ventricular myocytes that have aberrant electrical behavior. As such, VT is usually caused by underlying cardiac disease.",True,Ventricular Tachycardia,,,,
9f430e17-3a98-4181-b8c6-83dfb0c14b5b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Like a PVC, the aberrant depolarizations do not follow the normal conduction pathways so are wide (>120 msecs), but unlike a PVC, VT involves a ventricular rate >100 bpm. With disorganized contractility and reduced filling time, VT can lead to hemodynamic instability and severe hypotension—hence it is life threatening.",True,Ventricular Tachycardia,,,,
25ac86c4-f200-4010-a44f-ef049b528a97,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The QRS morphology in VT is highly variable between patients and depends on where the arrhythmia originates. Consequently there are several ways to classify VT based on duration, symptoms, QRS morphology, rate, and origin.",True,Ventricular Tachycardia,,,,
6045898d-b249-4d9d-9006-787edffc229d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Sustained VT is any VT that lasts for more than 30 seconds or is symptomatic. Nonsustained VT lasts for less than 30 seconds and is asymptomatic.,True,Ventricular Tachycardia,,,,
ddd0e581-29a5-4805-a9fa-d00f3795eab8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ddd0e581-29a5-4805-a9fa-d00f3795eab8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ddd0e581-29a5-4805-a9fa-d00f3795eab8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ddd0e581-29a5-4805-a9fa-d00f3795eab8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ddd0e581-29a5-4805-a9fa-d00f3795eab8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ddd0e581-29a5-4805-a9fa-d00f3795eab8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ddd0e581-29a5-4805-a9fa-d00f3795eab8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ddd0e581-29a5-4805-a9fa-d00f3795eab8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ddd0e581-29a5-4805-a9fa-d00f3795eab8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ddd0e581-29a5-4805-a9fa-d00f3795eab8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ddd0e581-29a5-4805-a9fa-d00f3795eab8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ddd0e581-29a5-4805-a9fa-d00f3795eab8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ddd0e581-29a5-4805-a9fa-d00f3795eab8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ddd0e581-29a5-4805-a9fa-d00f3795eab8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ddd0e581-29a5-4805-a9fa-d00f3795eab8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ddd0e581-29a5-4805-a9fa-d00f3795eab8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
ddd0e581-29a5-4805-a9fa-d00f3795eab8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
f23a7745-3625-4f52-b80b-3aacd3774d3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
f23a7745-3625-4f52-b80b-3aacd3774d3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
f23a7745-3625-4f52-b80b-3aacd3774d3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
f23a7745-3625-4f52-b80b-3aacd3774d3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
f23a7745-3625-4f52-b80b-3aacd3774d3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
f23a7745-3625-4f52-b80b-3aacd3774d3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
f23a7745-3625-4f52-b80b-3aacd3774d3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
f23a7745-3625-4f52-b80b-3aacd3774d3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
f23a7745-3625-4f52-b80b-3aacd3774d3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
f23a7745-3625-4f52-b80b-3aacd3774d3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
f23a7745-3625-4f52-b80b-3aacd3774d3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
f23a7745-3625-4f52-b80b-3aacd3774d3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
f23a7745-3625-4f52-b80b-3aacd3774d3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
f23a7745-3625-4f52-b80b-3aacd3774d3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
f23a7745-3625-4f52-b80b-3aacd3774d3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
f23a7745-3625-4f52-b80b-3aacd3774d3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
f23a7745-3625-4f52-b80b-3aacd3774d3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
33d69bfd-211b-4d23-b195-423c61e65c27,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Torsades de pointes is associated with a prolonged QT interval (>600 msecs) that helps distinguish it from other forms of polymorphous VT. The longer QT interval can be caused by ionic abnormalities that reduce the repolarizing current of Phase 3 of the cardiac action potential. This makes the myocardium susceptible to early after-depolarizations—the trigger for torsades de pointes. These after-depolarizations do not happen uniformly across the myocardium and are more common in endocardial tissue where the repolarization currents are slower. So torsades de pointes arises from the after-depolarizations causing reentry currents in neighboring tissue.,True,Ventricular Tachycardia,,,,
21a14a98-f9c3-4e89-b168-73a2017a9793,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Both common garden variety VTs and torsades de pointes can progress to ventricular fibrillation.,True,Ventricular Tachycardia,,,,
500cb708-7c45-46b2-b1b1-f2e526186f45,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Table 1.8: VT summary.,True,Ventricular Tachycardia,,,,
864a40b2-9d4b-4470-8328-8b84778cb39c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Ventricular Fibrillation,False,Ventricular Fibrillation,,,,
923d253a-1593-4a4a-afbf-e01d149c2817,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Ventricular fibrillation (VF) occurs when the ventricular rate exceeds 400 bpm. The disorganized and uncoordinated contraction of the myocardium causes cardiac output to fall to catastrophic levels. Rates of survival for out-of-hospital VF are low.,True,Ventricular Fibrillation,,,,
3043e256-c7bc-42ec-9fc7-354b4a506785,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3043e256-c7bc-42ec-9fc7-354b4a506785,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3043e256-c7bc-42ec-9fc7-354b4a506785,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3043e256-c7bc-42ec-9fc7-354b4a506785,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3043e256-c7bc-42ec-9fc7-354b4a506785,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3043e256-c7bc-42ec-9fc7-354b4a506785,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3043e256-c7bc-42ec-9fc7-354b4a506785,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3043e256-c7bc-42ec-9fc7-354b4a506785,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3043e256-c7bc-42ec-9fc7-354b4a506785,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3043e256-c7bc-42ec-9fc7-354b4a506785,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3043e256-c7bc-42ec-9fc7-354b4a506785,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3043e256-c7bc-42ec-9fc7-354b4a506785,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3043e256-c7bc-42ec-9fc7-354b4a506785,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3043e256-c7bc-42ec-9fc7-354b4a506785,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3043e256-c7bc-42ec-9fc7-354b4a506785,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3043e256-c7bc-42ec-9fc7-354b4a506785,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
3043e256-c7bc-42ec-9fc7-354b4a506785,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
d8b0a565-861d-420b-8bb4-aaefa9a041db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Table 1.9: VF summary.,True,Ventricular Fibrillation,,,,
b81e05dd-0da5-4009-a27a-321df2687523,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,First-Degree Atrioventricular Block,False,First-Degree Atrioventricular Block,,,,
8eb29914-f181-4562-9531-2d72b79ad8bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8eb29914-f181-4562-9531-2d72b79ad8bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8eb29914-f181-4562-9531-2d72b79ad8bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8eb29914-f181-4562-9531-2d72b79ad8bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8eb29914-f181-4562-9531-2d72b79ad8bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8eb29914-f181-4562-9531-2d72b79ad8bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8eb29914-f181-4562-9531-2d72b79ad8bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8eb29914-f181-4562-9531-2d72b79ad8bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8eb29914-f181-4562-9531-2d72b79ad8bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8eb29914-f181-4562-9531-2d72b79ad8bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8eb29914-f181-4562-9531-2d72b79ad8bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8eb29914-f181-4562-9531-2d72b79ad8bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8eb29914-f181-4562-9531-2d72b79ad8bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8eb29914-f181-4562-9531-2d72b79ad8bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8eb29914-f181-4562-9531-2d72b79ad8bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8eb29914-f181-4562-9531-2d72b79ad8bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8eb29914-f181-4562-9531-2d72b79ad8bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
4879b4fb-224a-4a9f-a66a-1b38fa35981b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
4879b4fb-224a-4a9f-a66a-1b38fa35981b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
4879b4fb-224a-4a9f-a66a-1b38fa35981b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
4879b4fb-224a-4a9f-a66a-1b38fa35981b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
4879b4fb-224a-4a9f-a66a-1b38fa35981b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
4879b4fb-224a-4a9f-a66a-1b38fa35981b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
4879b4fb-224a-4a9f-a66a-1b38fa35981b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
4879b4fb-224a-4a9f-a66a-1b38fa35981b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
4879b4fb-224a-4a9f-a66a-1b38fa35981b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
4879b4fb-224a-4a9f-a66a-1b38fa35981b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
4879b4fb-224a-4a9f-a66a-1b38fa35981b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
4879b4fb-224a-4a9f-a66a-1b38fa35981b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
4879b4fb-224a-4a9f-a66a-1b38fa35981b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
4879b4fb-224a-4a9f-a66a-1b38fa35981b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
4879b4fb-224a-4a9f-a66a-1b38fa35981b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
4879b4fb-224a-4a9f-a66a-1b38fa35981b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
4879b4fb-224a-4a9f-a66a-1b38fa35981b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
39953dd7-81b3-48f2-aac3-091a756a30ed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Table 1.10: First-degree block summary.,True,First-Degree Atrioventricular Block,,,,
4fb3fa92-5ac1-4ddb-9ba1-069a0a29ac9f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Second-Degree Atrioventricular Block,False,Second-Degree Atrioventricular Block,,,,
21accc12-121c-4a4e-aa23-03f11efffeab,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A second-degree atrioventricular block also has changes in P-R interval, but it starts to show failure of the P-wave to propagate a QRS complex every time (i.e., intermittently the depolarization fails to reach the ventricles). The pattern of missed ventricular depolarizations, or blocked P-waves, is often very regular and described as a ratio of P-waves to QRS complex. The way in which the P-R interval changes in relation to the blocked P-waves produces subclassifications of second-degree blocks, Mobitz I and II.",True,Second-Degree Atrioventricular Block,,,,
5f8fbc72-fe9d-4a5d-be74-11c566a02eba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
5f8fbc72-fe9d-4a5d-be74-11c566a02eba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
5f8fbc72-fe9d-4a5d-be74-11c566a02eba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
5f8fbc72-fe9d-4a5d-be74-11c566a02eba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
5f8fbc72-fe9d-4a5d-be74-11c566a02eba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
5f8fbc72-fe9d-4a5d-be74-11c566a02eba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
5f8fbc72-fe9d-4a5d-be74-11c566a02eba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
5f8fbc72-fe9d-4a5d-be74-11c566a02eba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
5f8fbc72-fe9d-4a5d-be74-11c566a02eba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
5f8fbc72-fe9d-4a5d-be74-11c566a02eba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
5f8fbc72-fe9d-4a5d-be74-11c566a02eba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
5f8fbc72-fe9d-4a5d-be74-11c566a02eba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
5f8fbc72-fe9d-4a5d-be74-11c566a02eba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
5f8fbc72-fe9d-4a5d-be74-11c566a02eba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
5f8fbc72-fe9d-4a5d-be74-11c566a02eba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
5f8fbc72-fe9d-4a5d-be74-11c566a02eba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
5f8fbc72-fe9d-4a5d-be74-11c566a02eba,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
a36e711e-39c8-4a43-8d2e-6c2f59aaa5e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a36e711e-39c8-4a43-8d2e-6c2f59aaa5e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a36e711e-39c8-4a43-8d2e-6c2f59aaa5e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a36e711e-39c8-4a43-8d2e-6c2f59aaa5e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a36e711e-39c8-4a43-8d2e-6c2f59aaa5e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a36e711e-39c8-4a43-8d2e-6c2f59aaa5e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a36e711e-39c8-4a43-8d2e-6c2f59aaa5e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a36e711e-39c8-4a43-8d2e-6c2f59aaa5e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a36e711e-39c8-4a43-8d2e-6c2f59aaa5e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a36e711e-39c8-4a43-8d2e-6c2f59aaa5e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a36e711e-39c8-4a43-8d2e-6c2f59aaa5e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a36e711e-39c8-4a43-8d2e-6c2f59aaa5e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a36e711e-39c8-4a43-8d2e-6c2f59aaa5e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a36e711e-39c8-4a43-8d2e-6c2f59aaa5e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a36e711e-39c8-4a43-8d2e-6c2f59aaa5e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a36e711e-39c8-4a43-8d2e-6c2f59aaa5e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a36e711e-39c8-4a43-8d2e-6c2f59aaa5e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
48c8162a-1763-4bcb-9070-30e791f05020,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Table 1.11: Second-degree block summary.,True,Second-Degree Atrioventricular Block,,,,
f102104a-6866-4616-8f11-7174ba3795f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Third-Degree Atrioventricular Block,False,Third-Degree Atrioventricular Block,,,,
06ae5a6e-ee9b-4922-95c5-a557b7c91cdf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
06ae5a6e-ee9b-4922-95c5-a557b7c91cdf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
06ae5a6e-ee9b-4922-95c5-a557b7c91cdf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
06ae5a6e-ee9b-4922-95c5-a557b7c91cdf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
06ae5a6e-ee9b-4922-95c5-a557b7c91cdf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
06ae5a6e-ee9b-4922-95c5-a557b7c91cdf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
06ae5a6e-ee9b-4922-95c5-a557b7c91cdf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
06ae5a6e-ee9b-4922-95c5-a557b7c91cdf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
06ae5a6e-ee9b-4922-95c5-a557b7c91cdf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
06ae5a6e-ee9b-4922-95c5-a557b7c91cdf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
06ae5a6e-ee9b-4922-95c5-a557b7c91cdf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
06ae5a6e-ee9b-4922-95c5-a557b7c91cdf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
06ae5a6e-ee9b-4922-95c5-a557b7c91cdf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
06ae5a6e-ee9b-4922-95c5-a557b7c91cdf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
06ae5a6e-ee9b-4922-95c5-a557b7c91cdf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
06ae5a6e-ee9b-4922-95c5-a557b7c91cdf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
06ae5a6e-ee9b-4922-95c5-a557b7c91cdf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
c99786a8-6d06-4669-a76c-09b23fd5f397,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Table 1.12: Third-degree block summary.,True,Third-Degree Atrioventricular Block,,,,
d6fb1d10-4df7-4890-a2d4-f722b1089c3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Left Bundle Branch Block,False,Left Bundle Branch Block,,,,
d98d7497-ae87-4a53-829c-0f811c0fac38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"A left bundle branch block (LBBB) is generated when the conductivity of the His-Purkinje system in the left ventricle is compromised, either through damage or disease. The ECG changes, and criteria for LBBB relate to these changes in conductivity and the left-side location.",True,Left Bundle Branch Block,,,,
1596fa6c-7715-41aa-b916-8c9087d3c74c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
1596fa6c-7715-41aa-b916-8c9087d3c74c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
1596fa6c-7715-41aa-b916-8c9087d3c74c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
1596fa6c-7715-41aa-b916-8c9087d3c74c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
1596fa6c-7715-41aa-b916-8c9087d3c74c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
1596fa6c-7715-41aa-b916-8c9087d3c74c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
1596fa6c-7715-41aa-b916-8c9087d3c74c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
1596fa6c-7715-41aa-b916-8c9087d3c74c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
1596fa6c-7715-41aa-b916-8c9087d3c74c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
1596fa6c-7715-41aa-b916-8c9087d3c74c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
1596fa6c-7715-41aa-b916-8c9087d3c74c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
1596fa6c-7715-41aa-b916-8c9087d3c74c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
1596fa6c-7715-41aa-b916-8c9087d3c74c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
1596fa6c-7715-41aa-b916-8c9087d3c74c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
1596fa6c-7715-41aa-b916-8c9087d3c74c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
1596fa6c-7715-41aa-b916-8c9087d3c74c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
1596fa6c-7715-41aa-b916-8c9087d3c74c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
f19ba488-dbff-4f47-b83f-8e2d4954a25b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The lateral leads (I, V5, and V6) normally show a downward deflecting Q-wave as normal septal deflection initially occurs left-to-right (i.e., away from the lateral leads). In LBBB the change in direction to right-to-left, plus the longer duration, eliminates the Q-wave from the lateral leads, and Q-waves will be small in aVL.",True,Left Bundle Branch Block,,,,
0e139b29-adc5-4280-a5fe-a9295e7ab59a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
0e139b29-adc5-4280-a5fe-a9295e7ab59a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
0e139b29-adc5-4280-a5fe-a9295e7ab59a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
0e139b29-adc5-4280-a5fe-a9295e7ab59a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
0e139b29-adc5-4280-a5fe-a9295e7ab59a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
0e139b29-adc5-4280-a5fe-a9295e7ab59a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
0e139b29-adc5-4280-a5fe-a9295e7ab59a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
0e139b29-adc5-4280-a5fe-a9295e7ab59a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
0e139b29-adc5-4280-a5fe-a9295e7ab59a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
0e139b29-adc5-4280-a5fe-a9295e7ab59a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
0e139b29-adc5-4280-a5fe-a9295e7ab59a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
0e139b29-adc5-4280-a5fe-a9295e7ab59a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
0e139b29-adc5-4280-a5fe-a9295e7ab59a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
0e139b29-adc5-4280-a5fe-a9295e7ab59a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
0e139b29-adc5-4280-a5fe-a9295e7ab59a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
0e139b29-adc5-4280-a5fe-a9295e7ab59a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
0e139b29-adc5-4280-a5fe-a9295e7ab59a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
70869406-92af-49c4-99ef-7378601cf9ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
70869406-92af-49c4-99ef-7378601cf9ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
70869406-92af-49c4-99ef-7378601cf9ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
70869406-92af-49c4-99ef-7378601cf9ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
70869406-92af-49c4-99ef-7378601cf9ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
70869406-92af-49c4-99ef-7378601cf9ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
70869406-92af-49c4-99ef-7378601cf9ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
70869406-92af-49c4-99ef-7378601cf9ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
70869406-92af-49c4-99ef-7378601cf9ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
70869406-92af-49c4-99ef-7378601cf9ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
70869406-92af-49c4-99ef-7378601cf9ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
70869406-92af-49c4-99ef-7378601cf9ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
70869406-92af-49c4-99ef-7378601cf9ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
70869406-92af-49c4-99ef-7378601cf9ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
70869406-92af-49c4-99ef-7378601cf9ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
70869406-92af-49c4-99ef-7378601cf9ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
70869406-92af-49c4-99ef-7378601cf9ac,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
45d8e93c-9b30-4e41-a717-09124f4dff80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Table 1.13: LBBB summary.,True,Left Bundle Branch Block,,,,
485a04d0-e283-4ec8-a294-73551f0358e9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Right Bundle Branch Block,False,Right Bundle Branch Block,,,,
407487b3-926e-431d-b8a1-48a59f249f80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The causes and manifestations of a right bundle branch block (RBBB) bear some similarities to those described for LBBB, but of course this time its depolarization of the right ventricle is delayed. Causes of RBBB include ischemic heart disease again as well as other myocardial diseases, but pulmonary issues such as pulmonary embolism and cor pulmonale can be added to the list.",True,Right Bundle Branch Block,,,,
d0d494a6-2f57-4ead-9389-58eef52c5b98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
d0d494a6-2f57-4ead-9389-58eef52c5b98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
d0d494a6-2f57-4ead-9389-58eef52c5b98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
d0d494a6-2f57-4ead-9389-58eef52c5b98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
d0d494a6-2f57-4ead-9389-58eef52c5b98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
d0d494a6-2f57-4ead-9389-58eef52c5b98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
d0d494a6-2f57-4ead-9389-58eef52c5b98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
d0d494a6-2f57-4ead-9389-58eef52c5b98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
d0d494a6-2f57-4ead-9389-58eef52c5b98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
d0d494a6-2f57-4ead-9389-58eef52c5b98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
d0d494a6-2f57-4ead-9389-58eef52c5b98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
d0d494a6-2f57-4ead-9389-58eef52c5b98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
d0d494a6-2f57-4ead-9389-58eef52c5b98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
d0d494a6-2f57-4ead-9389-58eef52c5b98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
d0d494a6-2f57-4ead-9389-58eef52c5b98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
d0d494a6-2f57-4ead-9389-58eef52c5b98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
d0d494a6-2f57-4ead-9389-58eef52c5b98,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
624e42d4-2a5b-454f-9328-28ac80ecf202,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Table 1.14: RBBB summary.,True,Right Bundle Branch Block,,,,
e8ddec94-6dfb-497d-946a-4e827292009d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Wolff-Parkinson-White Syndrome,False,Wolff-Parkinson-White Syndrome,,,,
b57b04f0-7c8c-4ae7-84fb-53f8979334fd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Normally the only electrical connection between the atria and the ventricles is the AV node. Otherwise the fibrous skeleton of the heart electrically insulates the atria from the ventricles. In Wolff-Parkinson-White (WPW) syndrome, that insulation is incomplete, and an “accessory pathway” connects the electrical system of the atria directly to the ventricles. If you think of the AV node as a bridge over the fibrous wall with regulated access, the accessory pathway is like a pathological tunnel under it with no regulation.",True,Wolff-Parkinson-White Syndrome,,,,
c2710cdf-b238-40a5-a1cc-2eb85173a098,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c2710cdf-b238-40a5-a1cc-2eb85173a098,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c2710cdf-b238-40a5-a1cc-2eb85173a098,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c2710cdf-b238-40a5-a1cc-2eb85173a098,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c2710cdf-b238-40a5-a1cc-2eb85173a098,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c2710cdf-b238-40a5-a1cc-2eb85173a098,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c2710cdf-b238-40a5-a1cc-2eb85173a098,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c2710cdf-b238-40a5-a1cc-2eb85173a098,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c2710cdf-b238-40a5-a1cc-2eb85173a098,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c2710cdf-b238-40a5-a1cc-2eb85173a098,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c2710cdf-b238-40a5-a1cc-2eb85173a098,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c2710cdf-b238-40a5-a1cc-2eb85173a098,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c2710cdf-b238-40a5-a1cc-2eb85173a098,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c2710cdf-b238-40a5-a1cc-2eb85173a098,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c2710cdf-b238-40a5-a1cc-2eb85173a098,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c2710cdf-b238-40a5-a1cc-2eb85173a098,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
c2710cdf-b238-40a5-a1cc-2eb85173a098,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
ab02c4af-87c4-4fc7-8df4-f736a422e079,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"WPW syndrome is often asymptomatic, and patients do not require immediate treatment. However, if atrial fibrillation occurs in a WPW patient, the accessory pathway can allow the atrial fibrillation waves through to the ventricle (with no AV nodal refractory period to prevent them). Consequently a high ventricular rate is seen, and the risk of ventricular fibrillation being established means immediate clinical attention is required.",True,Wolff-Parkinson-White Syndrome,,,,
bd4490d9-54d8-4573-ad81-12aaf3677ae1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Hyper- and Hypocalcemia,False,Hyper- and Hypocalcemia,,,,
72d4d7e4-68ce-48df-861d-47ebbef19e10,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
72d4d7e4-68ce-48df-861d-47ebbef19e10,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
72d4d7e4-68ce-48df-861d-47ebbef19e10,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
72d4d7e4-68ce-48df-861d-47ebbef19e10,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
72d4d7e4-68ce-48df-861d-47ebbef19e10,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
72d4d7e4-68ce-48df-861d-47ebbef19e10,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
72d4d7e4-68ce-48df-861d-47ebbef19e10,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
72d4d7e4-68ce-48df-861d-47ebbef19e10,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
72d4d7e4-68ce-48df-861d-47ebbef19e10,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
72d4d7e4-68ce-48df-861d-47ebbef19e10,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
72d4d7e4-68ce-48df-861d-47ebbef19e10,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
72d4d7e4-68ce-48df-861d-47ebbef19e10,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
72d4d7e4-68ce-48df-861d-47ebbef19e10,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
72d4d7e4-68ce-48df-861d-47ebbef19e10,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
72d4d7e4-68ce-48df-861d-47ebbef19e10,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
72d4d7e4-68ce-48df-861d-47ebbef19e10,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
72d4d7e4-68ce-48df-861d-47ebbef19e10,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
ee7e632a-a5a8-4ed3-9097-1c3d563fa6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
ee7e632a-a5a8-4ed3-9097-1c3d563fa6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
ee7e632a-a5a8-4ed3-9097-1c3d563fa6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
ee7e632a-a5a8-4ed3-9097-1c3d563fa6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
ee7e632a-a5a8-4ed3-9097-1c3d563fa6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
ee7e632a-a5a8-4ed3-9097-1c3d563fa6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
ee7e632a-a5a8-4ed3-9097-1c3d563fa6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
ee7e632a-a5a8-4ed3-9097-1c3d563fa6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
ee7e632a-a5a8-4ed3-9097-1c3d563fa6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
ee7e632a-a5a8-4ed3-9097-1c3d563fa6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
ee7e632a-a5a8-4ed3-9097-1c3d563fa6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
ee7e632a-a5a8-4ed3-9097-1c3d563fa6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
ee7e632a-a5a8-4ed3-9097-1c3d563fa6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
ee7e632a-a5a8-4ed3-9097-1c3d563fa6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
ee7e632a-a5a8-4ed3-9097-1c3d563fa6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
ee7e632a-a5a8-4ed3-9097-1c3d563fa6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
ee7e632a-a5a8-4ed3-9097-1c3d563fa6a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
6b40bea3-d82f-4830-ad4c-336fa929758f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Table 1.16: Hyper- and hypocalcemia summary.,True,Hyper- and Hypocalcemia,,,,
cc67fb03-04a3-4525-b7e8-1f0b4645bb46,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Hyper- and Hypokalemia,False,Hyper- and Hypokalemia,,,,
7d9c3314-aaa2-4d64-9b7c-e67f76a00f71,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"The pathophysiology is not as simple as changes in extracellular K+ changing the electrochemical gradient for K+. Because of potassium’s role in maintaining the resting membrane potential, shifts in extracellular potassium can also influence the activity of Na+ and Ca++ channels.",True,Hyper- and Hypokalemia,,,,
ba844da1-c484-4984-a6fe-a8190589364e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ba844da1-c484-4984-a6fe-a8190589364e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ba844da1-c484-4984-a6fe-a8190589364e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ba844da1-c484-4984-a6fe-a8190589364e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ba844da1-c484-4984-a6fe-a8190589364e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ba844da1-c484-4984-a6fe-a8190589364e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ba844da1-c484-4984-a6fe-a8190589364e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ba844da1-c484-4984-a6fe-a8190589364e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ba844da1-c484-4984-a6fe-a8190589364e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ba844da1-c484-4984-a6fe-a8190589364e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ba844da1-c484-4984-a6fe-a8190589364e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ba844da1-c484-4984-a6fe-a8190589364e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ba844da1-c484-4984-a6fe-a8190589364e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ba844da1-c484-4984-a6fe-a8190589364e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ba844da1-c484-4984-a6fe-a8190589364e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ba844da1-c484-4984-a6fe-a8190589364e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ba844da1-c484-4984-a6fe-a8190589364e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
d09e11af-5f7c-4fc8-9a0c-b6e73df1981a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"As hypokalemia also inhibits Na+-K+ ATPase, Na+ accumulates inside the cell. This in turn leads to an accumulation of Ca++ because of a subsequent failure of the Na+-Ca++ exchanger. Extended presence of these two positive ions inside the myocyte prolongs the action potential and may manifest as an increased width and amplitude of the P-wave.",True,Hyper- and Hypokalemia,,,,
9cbc386c-88c5-4b6b-b1d5-a9c9751e7ae0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"As hypokalemia worsens, the problems with K+ conductance and repolarization increase, and the myocardium becomes susceptible to early after-depolarization (EAD) arrhythmias.",True,Hyper- and Hypokalemia,,,,
0ef23842-85d5-4910-9582-1bdab37e67b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
0ef23842-85d5-4910-9582-1bdab37e67b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
0ef23842-85d5-4910-9582-1bdab37e67b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
0ef23842-85d5-4910-9582-1bdab37e67b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
0ef23842-85d5-4910-9582-1bdab37e67b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
0ef23842-85d5-4910-9582-1bdab37e67b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
0ef23842-85d5-4910-9582-1bdab37e67b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
0ef23842-85d5-4910-9582-1bdab37e67b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
0ef23842-85d5-4910-9582-1bdab37e67b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
0ef23842-85d5-4910-9582-1bdab37e67b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
0ef23842-85d5-4910-9582-1bdab37e67b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
0ef23842-85d5-4910-9582-1bdab37e67b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
0ef23842-85d5-4910-9582-1bdab37e67b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
0ef23842-85d5-4910-9582-1bdab37e67b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
0ef23842-85d5-4910-9582-1bdab37e67b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
0ef23842-85d5-4910-9582-1bdab37e67b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
0ef23842-85d5-4910-9582-1bdab37e67b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
503b6296-e5e4-4440-bfa1-0e3caa86d5ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
503b6296-e5e4-4440-bfa1-0e3caa86d5ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
503b6296-e5e4-4440-bfa1-0e3caa86d5ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
503b6296-e5e4-4440-bfa1-0e3caa86d5ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
503b6296-e5e4-4440-bfa1-0e3caa86d5ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
503b6296-e5e4-4440-bfa1-0e3caa86d5ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
503b6296-e5e4-4440-bfa1-0e3caa86d5ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
503b6296-e5e4-4440-bfa1-0e3caa86d5ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
503b6296-e5e4-4440-bfa1-0e3caa86d5ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
503b6296-e5e4-4440-bfa1-0e3caa86d5ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
503b6296-e5e4-4440-bfa1-0e3caa86d5ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
503b6296-e5e4-4440-bfa1-0e3caa86d5ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
503b6296-e5e4-4440-bfa1-0e3caa86d5ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
503b6296-e5e4-4440-bfa1-0e3caa86d5ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
503b6296-e5e4-4440-bfa1-0e3caa86d5ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
503b6296-e5e4-4440-bfa1-0e3caa86d5ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
503b6296-e5e4-4440-bfa1-0e3caa86d5ad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
460cde39-f6b6-4165-bd2f-82b25bf71156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
460cde39-f6b6-4165-bd2f-82b25bf71156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
460cde39-f6b6-4165-bd2f-82b25bf71156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
460cde39-f6b6-4165-bd2f-82b25bf71156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
460cde39-f6b6-4165-bd2f-82b25bf71156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
460cde39-f6b6-4165-bd2f-82b25bf71156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
460cde39-f6b6-4165-bd2f-82b25bf71156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
460cde39-f6b6-4165-bd2f-82b25bf71156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
460cde39-f6b6-4165-bd2f-82b25bf71156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
460cde39-f6b6-4165-bd2f-82b25bf71156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
460cde39-f6b6-4165-bd2f-82b25bf71156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
460cde39-f6b6-4165-bd2f-82b25bf71156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
460cde39-f6b6-4165-bd2f-82b25bf71156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
460cde39-f6b6-4165-bd2f-82b25bf71156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
460cde39-f6b6-4165-bd2f-82b25bf71156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
460cde39-f6b6-4165-bd2f-82b25bf71156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
460cde39-f6b6-4165-bd2f-82b25bf71156,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
fd37d342-1317-4e66-b19c-1abb4e4e3ea2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fd37d342-1317-4e66-b19c-1abb4e4e3ea2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fd37d342-1317-4e66-b19c-1abb4e4e3ea2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fd37d342-1317-4e66-b19c-1abb4e4e3ea2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fd37d342-1317-4e66-b19c-1abb4e4e3ea2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fd37d342-1317-4e66-b19c-1abb4e4e3ea2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fd37d342-1317-4e66-b19c-1abb4e4e3ea2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fd37d342-1317-4e66-b19c-1abb4e4e3ea2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fd37d342-1317-4e66-b19c-1abb4e4e3ea2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fd37d342-1317-4e66-b19c-1abb4e4e3ea2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fd37d342-1317-4e66-b19c-1abb4e4e3ea2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fd37d342-1317-4e66-b19c-1abb4e4e3ea2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fd37d342-1317-4e66-b19c-1abb4e4e3ea2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fd37d342-1317-4e66-b19c-1abb4e4e3ea2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fd37d342-1317-4e66-b19c-1abb4e4e3ea2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fd37d342-1317-4e66-b19c-1abb4e4e3ea2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
fd37d342-1317-4e66-b19c-1abb4e4e3ea2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
edc7cfb4-c66d-4fca-ba41-e4232f20f054,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Table 1.17: Hypo- and hyperkalemia summary.,True,Hyper- and Hypokalemia,,,,
afee53c7-c282-4e71-bc6c-2eac8f760830,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"References, resources, and further reading",False,"References, resources, and further reading",,,,
53f3cd15-e3f0-4fcb-a5f8-f03dc7cb410e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,Text,False,Text,,,,
b7e67ea9-4812-492e-bdf5-da11e8718516,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Burns, Ed, and Robert Buttner. Hypercalcaemia. Lift in the Fast Lane, 2021. https://litfl.com/hypercalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
4fbfac8a-6795-4839-ac61-9f19ff558c1c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Burns, Ed, and Robert Buttner. Hypocalcaemia. Life in the Fast Lane, 2021. https://litfl.com/hypocalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
96a8f4e1-e182-449d-b65a-1b6a9e70f9e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Buttner, Robert, and Ed Burns. Hyperkalaemia. Life in the Fast Lane. https://litfl.com/hyperkalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
e159eb0a-d9eb-4175-b2e5-90165549261d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Buttner, Robert, and Ed Burns. Hypokalaemia. Life in the Fast Lane, 2021. https://litfl.com/hypokalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
64718a22-0ed4-46b3-8641-66b64e0bb899,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Chhabra, Lovely, Amandeep Goyal, and Michael D. Benham. Wolff Parkinson White Syndrome. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK554437/, CC BY 4.0.",True,Text,,,,
290f47ba-af2d-4ac3-8378-683483817c30,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Custer, Adam M., Varun S. Yelamanchili, and Sarah L. Lappin. Multifocal Atrial Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459152/, CC BY 4.0.",True,Text,,,,
7f3b2635-7aff-45a3-8dc3-b1466899ed46,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Farzam, Khashayar, and John R. Richards. Premature Ventricular Contraction. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532991/, CC BY 4.0.",True,Text,,,,
e8194066-9633-4f85-af11-0326999fd8ef,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Foth, Christopher, Manesh Kumar Gangwani, and Heidi Alvey. Ventricular Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532954/, CC BY 4.0.",True,Text,,,,
29116953-28ad-4487-9ed5-05847684c1f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Hafeez, Yamama, and Shamai A. Grossman. Sinus Bradycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK493201/, CC BY 4.0.",True,Text,,,,
208d5bbf-f82f-49f3-9ac2-495afc5b3da9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Harkness, Weston T., and Mary Hicks. Right Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK507872/, CC BY 4.0.",True,Text,,,,
1fe076bb-6062-4108-b73d-280ee9d1181e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Heaton, Joseph, and Srikanth Yandrapalli. Premature Atrial Contractions. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK559204/, CC BY 4.0.",True,Text,,,,
bd447c38-5001-44e7-8471-2d19370a8a24,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Kashou, Anthony H., Amandeep Goyal, Tran Nguyen, and Lovely Chhabra. Atrioventricular Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459147/, CC BY 4.0.",True,Text,,,,
1e88f743-7e93-47d9-8219-b6d3b8d53492,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,“Learn the Heart.” Healio. https://www.healio.com/cardiology/learn-the-heart.,True,Text,,,,
fdee8c03-4f3f-40fc-8392-062986f73af6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Ludhwani, Dipesh, Amandeep Goyal, and Mandar Jagtap. Ventricular Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK537120/, CC BY 4.0.",True,Text,,,,
12725ff0-f036-49ed-a7f0-7c553b737e81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Nesheiwat, Zeid, Amandeep Goyal, and Mandar Jagtap. Atrial Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK526072/, CC BY 4.0.",True,Text,,,,
4cbd3a37-6975-4f52-bbbf-e6df88584f84,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Pipilas, Daniel C., Bruce A. Koplan, and Leonard S. Lilly. “The Electrocardiogram.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 4. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
6f056177-e7a6-4bd2-bddd-86f907176636,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Rodriguez Ziccardi, Mary, Amandeep Goyal, and Christopher V. Maani. Atrial Flutter. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK540985/, CC BY 4.0.",True,Text,,,,
0e8c9efe-acca-4890-b945-65131089f229,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-4,"Scherbak, Dmitriy, and Gregory J. Hicks. Left Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK482167/, CC BY 4.0.",True,Text,,,,
fd9f9a98-8f1b-45a2-8d01-d69fcc8b1f6e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,USMLE,False,USMLE,,,,
cf779294-83fd-4b90-9733-6478dcc89dc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
cf779294-83fd-4b90-9733-6478dcc89dc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
cf779294-83fd-4b90-9733-6478dcc89dc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
cf779294-83fd-4b90-9733-6478dcc89dc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
cf779294-83fd-4b90-9733-6478dcc89dc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
cf779294-83fd-4b90-9733-6478dcc89dc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
cf779294-83fd-4b90-9733-6478dcc89dc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
cf779294-83fd-4b90-9733-6478dcc89dc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
cf779294-83fd-4b90-9733-6478dcc89dc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
cf779294-83fd-4b90-9733-6478dcc89dc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
cf779294-83fd-4b90-9733-6478dcc89dc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
cf779294-83fd-4b90-9733-6478dcc89dc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
cf779294-83fd-4b90-9733-6478dcc89dc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
cf779294-83fd-4b90-9733-6478dcc89dc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
cf779294-83fd-4b90-9733-6478dcc89dc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
cf779294-83fd-4b90-9733-6478dcc89dc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
cf779294-83fd-4b90-9733-6478dcc89dc8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
f596a978-6306-4790-b26d-fa4bfd5cb731,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,10q22,False,10q22,,,,
e58cb887-ee23-49b3-a8ab-d561ab6e5920,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,q24,False,q24,,,,
ad93f848-1b6b-44ec-ab3c-8f851836cb7e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,fibrillatory,False,fibrillatory,,,,
f5bd4c20-93ff-429d-9833-055020032dd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
f5bd4c20-93ff-429d-9833-055020032dd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
f5bd4c20-93ff-429d-9833-055020032dd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
f5bd4c20-93ff-429d-9833-055020032dd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
f5bd4c20-93ff-429d-9833-055020032dd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
f5bd4c20-93ff-429d-9833-055020032dd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
f5bd4c20-93ff-429d-9833-055020032dd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
f5bd4c20-93ff-429d-9833-055020032dd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
f5bd4c20-93ff-429d-9833-055020032dd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
f5bd4c20-93ff-429d-9833-055020032dd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
f5bd4c20-93ff-429d-9833-055020032dd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
f5bd4c20-93ff-429d-9833-055020032dd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
f5bd4c20-93ff-429d-9833-055020032dd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
f5bd4c20-93ff-429d-9833-055020032dd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
f5bd4c20-93ff-429d-9833-055020032dd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
f5bd4c20-93ff-429d-9833-055020032dd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
f5bd4c20-93ff-429d-9833-055020032dd8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
266cb05a-b420-4cd1-9f0f-65ade1f766dc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Table 1.1: Atrial fibrillation summary.,True,fibrillatory,,,,
3811845b-fada-48e9-946a-180edcf75705,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Atrial Flutter,False,Atrial Flutter,,,,
09bfb7f6-08fd-4ec9-bd49-85eeedf607de,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
09bfb7f6-08fd-4ec9-bd49-85eeedf607de,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
09bfb7f6-08fd-4ec9-bd49-85eeedf607de,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
09bfb7f6-08fd-4ec9-bd49-85eeedf607de,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
09bfb7f6-08fd-4ec9-bd49-85eeedf607de,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
09bfb7f6-08fd-4ec9-bd49-85eeedf607de,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
09bfb7f6-08fd-4ec9-bd49-85eeedf607de,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
09bfb7f6-08fd-4ec9-bd49-85eeedf607de,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
09bfb7f6-08fd-4ec9-bd49-85eeedf607de,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
09bfb7f6-08fd-4ec9-bd49-85eeedf607de,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
09bfb7f6-08fd-4ec9-bd49-85eeedf607de,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
09bfb7f6-08fd-4ec9-bd49-85eeedf607de,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
09bfb7f6-08fd-4ec9-bd49-85eeedf607de,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
09bfb7f6-08fd-4ec9-bd49-85eeedf607de,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
09bfb7f6-08fd-4ec9-bd49-85eeedf607de,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
09bfb7f6-08fd-4ec9-bd49-85eeedf607de,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
09bfb7f6-08fd-4ec9-bd49-85eeedf607de,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
97a61317-6140-4065-bb60-a1a273767a32,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,macroreentrant,False,macroreentrant,,,,
97f1ebad-3ef0-47e1-9eb8-6c675467ecc1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,cavotricuspid,False,cavotricuspid,,,,
baaa432b-466f-4007-a8bd-27fed0277858,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"As with atrial fibrillation, the AV node’s refractory period prevents most of the P-waves from progressing to the ventricle, but commonly the AV conduction will be 2-to-1, so with an atrial rate of 300 bpm the ventricular rate will be 150 bpm. Parasympathetic stimulation or changes in AV node refractoriness can modify how many P-waves pass into the ventricle, but the the resultant rhythm is “regularly irregular.” When the heart rate is elevated, then distinguishing flutter from fibrillation becomes challenging and slowing ventricular rate pharmaceutically (adenosine) helps the flutter waves reemerge for a definitive diagnosis to be made.",True,cavotricuspid,,,,
b27edc87-cfdc-40b5-81be-04996795e73e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Table 1.2: Atrial flutter summary.,True,cavotricuspid,,,,
6b1d6d25-4b3e-4442-af4d-45cca985a6c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Multifocal Atrial Tachycardia,False,Multifocal Atrial Tachycardia,,,,
9feb8c94-612e-429c-988a-51af6d268b15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
9feb8c94-612e-429c-988a-51af6d268b15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
9feb8c94-612e-429c-988a-51af6d268b15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
9feb8c94-612e-429c-988a-51af6d268b15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
9feb8c94-612e-429c-988a-51af6d268b15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
9feb8c94-612e-429c-988a-51af6d268b15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
9feb8c94-612e-429c-988a-51af6d268b15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
9feb8c94-612e-429c-988a-51af6d268b15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
9feb8c94-612e-429c-988a-51af6d268b15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
9feb8c94-612e-429c-988a-51af6d268b15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
9feb8c94-612e-429c-988a-51af6d268b15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
9feb8c94-612e-429c-988a-51af6d268b15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
9feb8c94-612e-429c-988a-51af6d268b15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
9feb8c94-612e-429c-988a-51af6d268b15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
9feb8c94-612e-429c-988a-51af6d268b15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
9feb8c94-612e-429c-988a-51af6d268b15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
9feb8c94-612e-429c-988a-51af6d268b15,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
e3dacb83-a68b-4745-ba22-d1ad475742f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"MAT frequently occurs in the setting of severe lung disease and, more specifically, during an exacerbation of lung disease. This rhythm is benign, and once the underlying lung disease is treated, it should resolve.",True,Multifocal Atrial Tachycardia,,,,
be176075-b1e7-4b8c-b153-d869166a46c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Table 1.3: MAT summary.,True,Multifocal Atrial Tachycardia,,,,
3a4d6fe5-3778-400f-852b-95768f5609c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Premature Atrial Contraction,False,Premature Atrial Contraction,,,,
eec8f6e1-fe57-4735-9dd2-dfe37f497df6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A premature atrial contraction (PAC) is generated by a depolarization instigated outside of the SA node. This produces an extra P-wave, and consequently a shortening from previous P-P intervals is seen. The aberrant P-wave also has a different morphology from a sinus P-wave because of its different anatomical origin.",True,Premature Atrial Contraction,,,,
6dbb901f-e100-4faf-b23a-432de6e87fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
6dbb901f-e100-4faf-b23a-432de6e87fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
6dbb901f-e100-4faf-b23a-432de6e87fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
6dbb901f-e100-4faf-b23a-432de6e87fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
6dbb901f-e100-4faf-b23a-432de6e87fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
6dbb901f-e100-4faf-b23a-432de6e87fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
6dbb901f-e100-4faf-b23a-432de6e87fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
6dbb901f-e100-4faf-b23a-432de6e87fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
6dbb901f-e100-4faf-b23a-432de6e87fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
6dbb901f-e100-4faf-b23a-432de6e87fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
6dbb901f-e100-4faf-b23a-432de6e87fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
6dbb901f-e100-4faf-b23a-432de6e87fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
6dbb901f-e100-4faf-b23a-432de6e87fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
6dbb901f-e100-4faf-b23a-432de6e87fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
6dbb901f-e100-4faf-b23a-432de6e87fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
6dbb901f-e100-4faf-b23a-432de6e87fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
6dbb901f-e100-4faf-b23a-432de6e87fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
4b64ec68-b892-490c-bd88-e682614d84b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"If a PAC occurs when the AV node has not yet recovered from its refractory period, the PAC will fail to conduct to the ventricles; meaning the PAC will not be followed by a QRS complex or the ectopic P-R interval will be prolonged. The ECG will show a premature, ectopic P-wave and then no QRS complex afterward. When this occurs along with bigeminy, the ECG can appear as if there is sinus bradycardia.",True,Premature Atrial Contraction,,,,
0154a01c-1bd7-4c77-8b08-66909417e551,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Table 1.4: PAC summary.,True,Premature Atrial Contraction,,,,
21df3b1b-2159-4d3e-8085-cb4704f54582,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Sinus Bradycardia,False,Sinus Bradycardia,,,,
4cedfb12-72c3-4a39-b1b3-eb079920ce1d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Sinus bradycardia denotes a sinus rhythm below 60 bpm. Otherwise the ECG waveform is normal on an ECG with an upright P-wave in lead II preceding every QRS complex. There are many intrinsic causes associated with the heart itself, as well as extrinsic causes, some of which are listed table 1.5. Sinus bradycardia is usually asymptomatic as rates of 40–50 bpm can maintain hemodynamic stability. Rates below this can produce symptoms of fatigue, dizziness, and dyspnea on exertion.",True,Sinus Bradycardia,,,,
1ea41c5f-3d0a-4738-8f67-5fc48a803c29,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Table 1.5: Intrinsic and extrinsic causes associated with the heart.,True,Sinus Bradycardia,,,,
aca71944-57ce-4c6b-a355-83c61aadd4e5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Table 1.6: Sinus bradycardia summary.,True,Sinus Bradycardia,,,,
643b5c88-b61e-43f4-a9c1-946746b9babc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Premature Ventricular Contractions,False,Premature Ventricular Contractions,,,,
16d33f7b-16c9-4894-b028-b5e68773077a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
16d33f7b-16c9-4894-b028-b5e68773077a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
16d33f7b-16c9-4894-b028-b5e68773077a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
16d33f7b-16c9-4894-b028-b5e68773077a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
16d33f7b-16c9-4894-b028-b5e68773077a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
16d33f7b-16c9-4894-b028-b5e68773077a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
16d33f7b-16c9-4894-b028-b5e68773077a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
16d33f7b-16c9-4894-b028-b5e68773077a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
16d33f7b-16c9-4894-b028-b5e68773077a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
16d33f7b-16c9-4894-b028-b5e68773077a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
16d33f7b-16c9-4894-b028-b5e68773077a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
16d33f7b-16c9-4894-b028-b5e68773077a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
16d33f7b-16c9-4894-b028-b5e68773077a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
16d33f7b-16c9-4894-b028-b5e68773077a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
16d33f7b-16c9-4894-b028-b5e68773077a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
16d33f7b-16c9-4894-b028-b5e68773077a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
16d33f7b-16c9-4894-b028-b5e68773077a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
c5facf8e-ccc2-4b08-9762-80a3f814a009,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Table 1.7: PVC summary.,True,Premature Ventricular Contractions,,,,
11c3b5d6-a021-4ec3-8578-dbabb4901053,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Ventricular Tachycardia,False,Ventricular Tachycardia,,,,
fe197b47-70ca-41c8-a4a7-c0c1b4d74092,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Ventricular tachycardia (VT) is caused by reentry currents being established in the ventricular myocardium or groups of ventricular myocytes that have aberrant electrical behavior. As such, VT is usually caused by underlying cardiac disease.",True,Ventricular Tachycardia,,,,
b88caf21-48e4-4025-90bd-9f49b9af6ac3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Like a PVC, the aberrant depolarizations do not follow the normal conduction pathways so are wide (>120 msecs), but unlike a PVC, VT involves a ventricular rate >100 bpm. With disorganized contractility and reduced filling time, VT can lead to hemodynamic instability and severe hypotension—hence it is life threatening.",True,Ventricular Tachycardia,,,,
784ab4ea-9798-42dc-a6ee-64f8986ee568,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The QRS morphology in VT is highly variable between patients and depends on where the arrhythmia originates. Consequently there are several ways to classify VT based on duration, symptoms, QRS morphology, rate, and origin.",True,Ventricular Tachycardia,,,,
ff17c3f4-c4bf-42f4-94fc-53333a272370,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Sustained VT is any VT that lasts for more than 30 seconds or is symptomatic. Nonsustained VT lasts for less than 30 seconds and is asymptomatic.,True,Ventricular Tachycardia,,,,
32222afa-27f3-4ca1-88c0-857bb1ccccbc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
32222afa-27f3-4ca1-88c0-857bb1ccccbc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
32222afa-27f3-4ca1-88c0-857bb1ccccbc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
32222afa-27f3-4ca1-88c0-857bb1ccccbc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
32222afa-27f3-4ca1-88c0-857bb1ccccbc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
32222afa-27f3-4ca1-88c0-857bb1ccccbc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
32222afa-27f3-4ca1-88c0-857bb1ccccbc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
32222afa-27f3-4ca1-88c0-857bb1ccccbc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
32222afa-27f3-4ca1-88c0-857bb1ccccbc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
32222afa-27f3-4ca1-88c0-857bb1ccccbc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
32222afa-27f3-4ca1-88c0-857bb1ccccbc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
32222afa-27f3-4ca1-88c0-857bb1ccccbc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
32222afa-27f3-4ca1-88c0-857bb1ccccbc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
32222afa-27f3-4ca1-88c0-857bb1ccccbc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
32222afa-27f3-4ca1-88c0-857bb1ccccbc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
32222afa-27f3-4ca1-88c0-857bb1ccccbc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
32222afa-27f3-4ca1-88c0-857bb1ccccbc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
55496287-2c48-491d-89f0-2e35fa602cd6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
55496287-2c48-491d-89f0-2e35fa602cd6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
55496287-2c48-491d-89f0-2e35fa602cd6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
55496287-2c48-491d-89f0-2e35fa602cd6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
55496287-2c48-491d-89f0-2e35fa602cd6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
55496287-2c48-491d-89f0-2e35fa602cd6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
55496287-2c48-491d-89f0-2e35fa602cd6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
55496287-2c48-491d-89f0-2e35fa602cd6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
55496287-2c48-491d-89f0-2e35fa602cd6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
55496287-2c48-491d-89f0-2e35fa602cd6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
55496287-2c48-491d-89f0-2e35fa602cd6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
55496287-2c48-491d-89f0-2e35fa602cd6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
55496287-2c48-491d-89f0-2e35fa602cd6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
55496287-2c48-491d-89f0-2e35fa602cd6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
55496287-2c48-491d-89f0-2e35fa602cd6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
55496287-2c48-491d-89f0-2e35fa602cd6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
55496287-2c48-491d-89f0-2e35fa602cd6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
6a8aac83-7736-45b1-8b37-845952a69a59,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Torsades de pointes is associated with a prolonged QT interval (>600 msecs) that helps distinguish it from other forms of polymorphous VT. The longer QT interval can be caused by ionic abnormalities that reduce the repolarizing current of Phase 3 of the cardiac action potential. This makes the myocardium susceptible to early after-depolarizations—the trigger for torsades de pointes. These after-depolarizations do not happen uniformly across the myocardium and are more common in endocardial tissue where the repolarization currents are slower. So torsades de pointes arises from the after-depolarizations causing reentry currents in neighboring tissue.,True,Ventricular Tachycardia,,,,
3ef78582-35ef-4c77-98c5-952da1cd246f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Both common garden variety VTs and torsades de pointes can progress to ventricular fibrillation.,True,Ventricular Tachycardia,,,,
97acb77a-dc02-4946-b8ff-e9a4382dca38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Table 1.8: VT summary.,True,Ventricular Tachycardia,,,,
5e2eb1b5-40b6-40dc-8e3e-4869587d46fa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Ventricular Fibrillation,False,Ventricular Fibrillation,,,,
1445a983-ddd8-4aea-a358-d122e7318c36,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Ventricular fibrillation (VF) occurs when the ventricular rate exceeds 400 bpm. The disorganized and uncoordinated contraction of the myocardium causes cardiac output to fall to catastrophic levels. Rates of survival for out-of-hospital VF are low.,True,Ventricular Fibrillation,,,,
341d1310-e6d5-418b-9616-4d7f05c1cc4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
341d1310-e6d5-418b-9616-4d7f05c1cc4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
341d1310-e6d5-418b-9616-4d7f05c1cc4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
341d1310-e6d5-418b-9616-4d7f05c1cc4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
341d1310-e6d5-418b-9616-4d7f05c1cc4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
341d1310-e6d5-418b-9616-4d7f05c1cc4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
341d1310-e6d5-418b-9616-4d7f05c1cc4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
341d1310-e6d5-418b-9616-4d7f05c1cc4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
341d1310-e6d5-418b-9616-4d7f05c1cc4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
341d1310-e6d5-418b-9616-4d7f05c1cc4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
341d1310-e6d5-418b-9616-4d7f05c1cc4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
341d1310-e6d5-418b-9616-4d7f05c1cc4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
341d1310-e6d5-418b-9616-4d7f05c1cc4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
341d1310-e6d5-418b-9616-4d7f05c1cc4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
341d1310-e6d5-418b-9616-4d7f05c1cc4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
341d1310-e6d5-418b-9616-4d7f05c1cc4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
341d1310-e6d5-418b-9616-4d7f05c1cc4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
51f67c42-9523-4f12-add3-9c7ad1abd043,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Table 1.9: VF summary.,True,Ventricular Fibrillation,,,,
24a69566-06d9-420c-852c-8f86de5458bc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,First-Degree Atrioventricular Block,False,First-Degree Atrioventricular Block,,,,
2085d2fb-225c-4775-adb0-7a3faaa2b66d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
2085d2fb-225c-4775-adb0-7a3faaa2b66d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
2085d2fb-225c-4775-adb0-7a3faaa2b66d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
2085d2fb-225c-4775-adb0-7a3faaa2b66d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
2085d2fb-225c-4775-adb0-7a3faaa2b66d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
2085d2fb-225c-4775-adb0-7a3faaa2b66d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
2085d2fb-225c-4775-adb0-7a3faaa2b66d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
2085d2fb-225c-4775-adb0-7a3faaa2b66d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
2085d2fb-225c-4775-adb0-7a3faaa2b66d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
2085d2fb-225c-4775-adb0-7a3faaa2b66d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
2085d2fb-225c-4775-adb0-7a3faaa2b66d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
2085d2fb-225c-4775-adb0-7a3faaa2b66d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
2085d2fb-225c-4775-adb0-7a3faaa2b66d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
2085d2fb-225c-4775-adb0-7a3faaa2b66d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
2085d2fb-225c-4775-adb0-7a3faaa2b66d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
2085d2fb-225c-4775-adb0-7a3faaa2b66d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
2085d2fb-225c-4775-adb0-7a3faaa2b66d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
99e4a3cb-bab4-444c-84f5-391cf9c8e121,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
99e4a3cb-bab4-444c-84f5-391cf9c8e121,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
99e4a3cb-bab4-444c-84f5-391cf9c8e121,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
99e4a3cb-bab4-444c-84f5-391cf9c8e121,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
99e4a3cb-bab4-444c-84f5-391cf9c8e121,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
99e4a3cb-bab4-444c-84f5-391cf9c8e121,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
99e4a3cb-bab4-444c-84f5-391cf9c8e121,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
99e4a3cb-bab4-444c-84f5-391cf9c8e121,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
99e4a3cb-bab4-444c-84f5-391cf9c8e121,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
99e4a3cb-bab4-444c-84f5-391cf9c8e121,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
99e4a3cb-bab4-444c-84f5-391cf9c8e121,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
99e4a3cb-bab4-444c-84f5-391cf9c8e121,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
99e4a3cb-bab4-444c-84f5-391cf9c8e121,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
99e4a3cb-bab4-444c-84f5-391cf9c8e121,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
99e4a3cb-bab4-444c-84f5-391cf9c8e121,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
99e4a3cb-bab4-444c-84f5-391cf9c8e121,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
99e4a3cb-bab4-444c-84f5-391cf9c8e121,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
4961451c-2e8e-47a9-82ed-14ea26b70d4c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Table 1.10: First-degree block summary.,True,First-Degree Atrioventricular Block,,,,
564163bc-02f5-428c-abc5-5621f21e544a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Second-Degree Atrioventricular Block,False,Second-Degree Atrioventricular Block,,,,
78fa4168-0d07-4196-ab2d-be78ad8fbc7f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A second-degree atrioventricular block also has changes in P-R interval, but it starts to show failure of the P-wave to propagate a QRS complex every time (i.e., intermittently the depolarization fails to reach the ventricles). The pattern of missed ventricular depolarizations, or blocked P-waves, is often very regular and described as a ratio of P-waves to QRS complex. The way in which the P-R interval changes in relation to the blocked P-waves produces subclassifications of second-degree blocks, Mobitz I and II.",True,Second-Degree Atrioventricular Block,,,,
690e6ac6-b309-429a-bcba-4cef264302a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
690e6ac6-b309-429a-bcba-4cef264302a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
690e6ac6-b309-429a-bcba-4cef264302a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
690e6ac6-b309-429a-bcba-4cef264302a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
690e6ac6-b309-429a-bcba-4cef264302a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
690e6ac6-b309-429a-bcba-4cef264302a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
690e6ac6-b309-429a-bcba-4cef264302a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
690e6ac6-b309-429a-bcba-4cef264302a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
690e6ac6-b309-429a-bcba-4cef264302a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
690e6ac6-b309-429a-bcba-4cef264302a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
690e6ac6-b309-429a-bcba-4cef264302a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
690e6ac6-b309-429a-bcba-4cef264302a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
690e6ac6-b309-429a-bcba-4cef264302a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
690e6ac6-b309-429a-bcba-4cef264302a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
690e6ac6-b309-429a-bcba-4cef264302a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
690e6ac6-b309-429a-bcba-4cef264302a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
690e6ac6-b309-429a-bcba-4cef264302a9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
a5db7197-8a44-4f57-b852-7418bf9f661a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a5db7197-8a44-4f57-b852-7418bf9f661a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a5db7197-8a44-4f57-b852-7418bf9f661a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a5db7197-8a44-4f57-b852-7418bf9f661a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a5db7197-8a44-4f57-b852-7418bf9f661a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a5db7197-8a44-4f57-b852-7418bf9f661a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a5db7197-8a44-4f57-b852-7418bf9f661a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a5db7197-8a44-4f57-b852-7418bf9f661a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a5db7197-8a44-4f57-b852-7418bf9f661a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a5db7197-8a44-4f57-b852-7418bf9f661a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a5db7197-8a44-4f57-b852-7418bf9f661a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a5db7197-8a44-4f57-b852-7418bf9f661a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a5db7197-8a44-4f57-b852-7418bf9f661a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a5db7197-8a44-4f57-b852-7418bf9f661a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a5db7197-8a44-4f57-b852-7418bf9f661a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a5db7197-8a44-4f57-b852-7418bf9f661a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a5db7197-8a44-4f57-b852-7418bf9f661a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
dd9abd6c-336a-4b9d-ada6-3cbc6e2beecb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Table 1.11: Second-degree block summary.,True,Second-Degree Atrioventricular Block,,,,
74f530ea-b7ee-4a36-bc3b-1fc6440383e2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Third-Degree Atrioventricular Block,False,Third-Degree Atrioventricular Block,,,,
bb1c14b6-c230-418c-8627-0620a095b6c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
bb1c14b6-c230-418c-8627-0620a095b6c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
bb1c14b6-c230-418c-8627-0620a095b6c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
bb1c14b6-c230-418c-8627-0620a095b6c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
bb1c14b6-c230-418c-8627-0620a095b6c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
bb1c14b6-c230-418c-8627-0620a095b6c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
bb1c14b6-c230-418c-8627-0620a095b6c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
bb1c14b6-c230-418c-8627-0620a095b6c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
bb1c14b6-c230-418c-8627-0620a095b6c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
bb1c14b6-c230-418c-8627-0620a095b6c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
bb1c14b6-c230-418c-8627-0620a095b6c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
bb1c14b6-c230-418c-8627-0620a095b6c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
bb1c14b6-c230-418c-8627-0620a095b6c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
bb1c14b6-c230-418c-8627-0620a095b6c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
bb1c14b6-c230-418c-8627-0620a095b6c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
bb1c14b6-c230-418c-8627-0620a095b6c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
bb1c14b6-c230-418c-8627-0620a095b6c4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
3f635610-3e06-4e53-8648-6018036a3354,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Table 1.12: Third-degree block summary.,True,Third-Degree Atrioventricular Block,,,,
c05aff29-bec0-4376-8f72-62a684f78f19,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Left Bundle Branch Block,False,Left Bundle Branch Block,,,,
88459c84-aed3-44ca-9d3d-4ec1def1d385,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"A left bundle branch block (LBBB) is generated when the conductivity of the His-Purkinje system in the left ventricle is compromised, either through damage or disease. The ECG changes, and criteria for LBBB relate to these changes in conductivity and the left-side location.",True,Left Bundle Branch Block,,,,
85159c84-a25d-4d82-9633-e3632ae8efb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
85159c84-a25d-4d82-9633-e3632ae8efb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
85159c84-a25d-4d82-9633-e3632ae8efb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
85159c84-a25d-4d82-9633-e3632ae8efb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
85159c84-a25d-4d82-9633-e3632ae8efb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
85159c84-a25d-4d82-9633-e3632ae8efb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
85159c84-a25d-4d82-9633-e3632ae8efb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
85159c84-a25d-4d82-9633-e3632ae8efb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
85159c84-a25d-4d82-9633-e3632ae8efb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
85159c84-a25d-4d82-9633-e3632ae8efb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
85159c84-a25d-4d82-9633-e3632ae8efb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
85159c84-a25d-4d82-9633-e3632ae8efb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
85159c84-a25d-4d82-9633-e3632ae8efb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
85159c84-a25d-4d82-9633-e3632ae8efb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
85159c84-a25d-4d82-9633-e3632ae8efb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
85159c84-a25d-4d82-9633-e3632ae8efb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
85159c84-a25d-4d82-9633-e3632ae8efb8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
cca973ad-21e2-4355-9e83-aee90e154410,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The lateral leads (I, V5, and V6) normally show a downward deflecting Q-wave as normal septal deflection initially occurs left-to-right (i.e., away from the lateral leads). In LBBB the change in direction to right-to-left, plus the longer duration, eliminates the Q-wave from the lateral leads, and Q-waves will be small in aVL.",True,Left Bundle Branch Block,,,,
986e9508-bcbe-4753-b1fc-3a66ad70a044,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
986e9508-bcbe-4753-b1fc-3a66ad70a044,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
986e9508-bcbe-4753-b1fc-3a66ad70a044,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
986e9508-bcbe-4753-b1fc-3a66ad70a044,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
986e9508-bcbe-4753-b1fc-3a66ad70a044,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
986e9508-bcbe-4753-b1fc-3a66ad70a044,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
986e9508-bcbe-4753-b1fc-3a66ad70a044,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
986e9508-bcbe-4753-b1fc-3a66ad70a044,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
986e9508-bcbe-4753-b1fc-3a66ad70a044,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
986e9508-bcbe-4753-b1fc-3a66ad70a044,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
986e9508-bcbe-4753-b1fc-3a66ad70a044,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
986e9508-bcbe-4753-b1fc-3a66ad70a044,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
986e9508-bcbe-4753-b1fc-3a66ad70a044,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
986e9508-bcbe-4753-b1fc-3a66ad70a044,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
986e9508-bcbe-4753-b1fc-3a66ad70a044,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
986e9508-bcbe-4753-b1fc-3a66ad70a044,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
986e9508-bcbe-4753-b1fc-3a66ad70a044,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
8c18a6f7-1ff1-40ef-a53b-627615d8bc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8c18a6f7-1ff1-40ef-a53b-627615d8bc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8c18a6f7-1ff1-40ef-a53b-627615d8bc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8c18a6f7-1ff1-40ef-a53b-627615d8bc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8c18a6f7-1ff1-40ef-a53b-627615d8bc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8c18a6f7-1ff1-40ef-a53b-627615d8bc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8c18a6f7-1ff1-40ef-a53b-627615d8bc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8c18a6f7-1ff1-40ef-a53b-627615d8bc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8c18a6f7-1ff1-40ef-a53b-627615d8bc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8c18a6f7-1ff1-40ef-a53b-627615d8bc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8c18a6f7-1ff1-40ef-a53b-627615d8bc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8c18a6f7-1ff1-40ef-a53b-627615d8bc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8c18a6f7-1ff1-40ef-a53b-627615d8bc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8c18a6f7-1ff1-40ef-a53b-627615d8bc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8c18a6f7-1ff1-40ef-a53b-627615d8bc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8c18a6f7-1ff1-40ef-a53b-627615d8bc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8c18a6f7-1ff1-40ef-a53b-627615d8bc99,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
93bb2eec-9c54-4ca3-9901-ccd6efc553cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Table 1.13: LBBB summary.,True,Left Bundle Branch Block,,,,
7d7b945d-6c0f-407d-9e3b-3d9614b61ba9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Right Bundle Branch Block,False,Right Bundle Branch Block,,,,
9f632c69-ffea-4147-a56f-581276ea1095,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The causes and manifestations of a right bundle branch block (RBBB) bear some similarities to those described for LBBB, but of course this time its depolarization of the right ventricle is delayed. Causes of RBBB include ischemic heart disease again as well as other myocardial diseases, but pulmonary issues such as pulmonary embolism and cor pulmonale can be added to the list.",True,Right Bundle Branch Block,,,,
3a8b2261-5346-4559-846a-f676686c3f58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
3a8b2261-5346-4559-846a-f676686c3f58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
3a8b2261-5346-4559-846a-f676686c3f58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
3a8b2261-5346-4559-846a-f676686c3f58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
3a8b2261-5346-4559-846a-f676686c3f58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
3a8b2261-5346-4559-846a-f676686c3f58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
3a8b2261-5346-4559-846a-f676686c3f58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
3a8b2261-5346-4559-846a-f676686c3f58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
3a8b2261-5346-4559-846a-f676686c3f58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
3a8b2261-5346-4559-846a-f676686c3f58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
3a8b2261-5346-4559-846a-f676686c3f58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
3a8b2261-5346-4559-846a-f676686c3f58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
3a8b2261-5346-4559-846a-f676686c3f58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
3a8b2261-5346-4559-846a-f676686c3f58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
3a8b2261-5346-4559-846a-f676686c3f58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
3a8b2261-5346-4559-846a-f676686c3f58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
3a8b2261-5346-4559-846a-f676686c3f58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
4cbab26d-baf8-446d-a30d-112f2353942a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Table 1.14: RBBB summary.,True,Right Bundle Branch Block,,,,
84a87f33-f2e1-4a75-969f-9840448429a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Wolff-Parkinson-White Syndrome,False,Wolff-Parkinson-White Syndrome,,,,
b37cd74a-661f-4381-a34b-7f2b30f165e7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Normally the only electrical connection between the atria and the ventricles is the AV node. Otherwise the fibrous skeleton of the heart electrically insulates the atria from the ventricles. In Wolff-Parkinson-White (WPW) syndrome, that insulation is incomplete, and an “accessory pathway” connects the electrical system of the atria directly to the ventricles. If you think of the AV node as a bridge over the fibrous wall with regulated access, the accessory pathway is like a pathological tunnel under it with no regulation.",True,Wolff-Parkinson-White Syndrome,,,,
629915c1-6da7-4167-b0cd-71357b82a1a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
629915c1-6da7-4167-b0cd-71357b82a1a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
629915c1-6da7-4167-b0cd-71357b82a1a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
629915c1-6da7-4167-b0cd-71357b82a1a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
629915c1-6da7-4167-b0cd-71357b82a1a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
629915c1-6da7-4167-b0cd-71357b82a1a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
629915c1-6da7-4167-b0cd-71357b82a1a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
629915c1-6da7-4167-b0cd-71357b82a1a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
629915c1-6da7-4167-b0cd-71357b82a1a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
629915c1-6da7-4167-b0cd-71357b82a1a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
629915c1-6da7-4167-b0cd-71357b82a1a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
629915c1-6da7-4167-b0cd-71357b82a1a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
629915c1-6da7-4167-b0cd-71357b82a1a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
629915c1-6da7-4167-b0cd-71357b82a1a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
629915c1-6da7-4167-b0cd-71357b82a1a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
629915c1-6da7-4167-b0cd-71357b82a1a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
629915c1-6da7-4167-b0cd-71357b82a1a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
9d0010ea-a5bc-45af-aa01-801cb1c9862f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"WPW syndrome is often asymptomatic, and patients do not require immediate treatment. However, if atrial fibrillation occurs in a WPW patient, the accessory pathway can allow the atrial fibrillation waves through to the ventricle (with no AV nodal refractory period to prevent them). Consequently a high ventricular rate is seen, and the risk of ventricular fibrillation being established means immediate clinical attention is required.",True,Wolff-Parkinson-White Syndrome,,,,
f6afd1e9-3066-4eca-864b-8599e6ada4be,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Hyper- and Hypocalcemia,False,Hyper- and Hypocalcemia,,,,
43cb13d6-9f7c-4330-b468-777519b154db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
43cb13d6-9f7c-4330-b468-777519b154db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
43cb13d6-9f7c-4330-b468-777519b154db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
43cb13d6-9f7c-4330-b468-777519b154db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
43cb13d6-9f7c-4330-b468-777519b154db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
43cb13d6-9f7c-4330-b468-777519b154db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
43cb13d6-9f7c-4330-b468-777519b154db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
43cb13d6-9f7c-4330-b468-777519b154db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
43cb13d6-9f7c-4330-b468-777519b154db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
43cb13d6-9f7c-4330-b468-777519b154db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
43cb13d6-9f7c-4330-b468-777519b154db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
43cb13d6-9f7c-4330-b468-777519b154db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
43cb13d6-9f7c-4330-b468-777519b154db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
43cb13d6-9f7c-4330-b468-777519b154db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
43cb13d6-9f7c-4330-b468-777519b154db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
43cb13d6-9f7c-4330-b468-777519b154db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
43cb13d6-9f7c-4330-b468-777519b154db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
cd81ef9f-f82c-4bc1-8548-bb608bd45094,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
cd81ef9f-f82c-4bc1-8548-bb608bd45094,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
cd81ef9f-f82c-4bc1-8548-bb608bd45094,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
cd81ef9f-f82c-4bc1-8548-bb608bd45094,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
cd81ef9f-f82c-4bc1-8548-bb608bd45094,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
cd81ef9f-f82c-4bc1-8548-bb608bd45094,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
cd81ef9f-f82c-4bc1-8548-bb608bd45094,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
cd81ef9f-f82c-4bc1-8548-bb608bd45094,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
cd81ef9f-f82c-4bc1-8548-bb608bd45094,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
cd81ef9f-f82c-4bc1-8548-bb608bd45094,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
cd81ef9f-f82c-4bc1-8548-bb608bd45094,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
cd81ef9f-f82c-4bc1-8548-bb608bd45094,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
cd81ef9f-f82c-4bc1-8548-bb608bd45094,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
cd81ef9f-f82c-4bc1-8548-bb608bd45094,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
cd81ef9f-f82c-4bc1-8548-bb608bd45094,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
cd81ef9f-f82c-4bc1-8548-bb608bd45094,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
cd81ef9f-f82c-4bc1-8548-bb608bd45094,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
c422f86a-3525-406a-860b-421f30e93f23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Table 1.16: Hyper- and hypocalcemia summary.,True,Hyper- and Hypocalcemia,,,,
8c32522f-bb3f-4278-afef-da9f426a2648,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Hyper- and Hypokalemia,False,Hyper- and Hypokalemia,,,,
41bf0c31-bea4-44ce-987c-91f900133051,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"The pathophysiology is not as simple as changes in extracellular K+ changing the electrochemical gradient for K+. Because of potassium’s role in maintaining the resting membrane potential, shifts in extracellular potassium can also influence the activity of Na+ and Ca++ channels.",True,Hyper- and Hypokalemia,,,,
60826dc5-0502-456a-a72b-07f29321eda5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
60826dc5-0502-456a-a72b-07f29321eda5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
60826dc5-0502-456a-a72b-07f29321eda5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
60826dc5-0502-456a-a72b-07f29321eda5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
60826dc5-0502-456a-a72b-07f29321eda5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
60826dc5-0502-456a-a72b-07f29321eda5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
60826dc5-0502-456a-a72b-07f29321eda5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
60826dc5-0502-456a-a72b-07f29321eda5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
60826dc5-0502-456a-a72b-07f29321eda5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
60826dc5-0502-456a-a72b-07f29321eda5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
60826dc5-0502-456a-a72b-07f29321eda5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
60826dc5-0502-456a-a72b-07f29321eda5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
60826dc5-0502-456a-a72b-07f29321eda5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
60826dc5-0502-456a-a72b-07f29321eda5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
60826dc5-0502-456a-a72b-07f29321eda5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
60826dc5-0502-456a-a72b-07f29321eda5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
60826dc5-0502-456a-a72b-07f29321eda5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
799c0c69-f8b2-427c-aacf-f9707f790269,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"As hypokalemia also inhibits Na+-K+ ATPase, Na+ accumulates inside the cell. This in turn leads to an accumulation of Ca++ because of a subsequent failure of the Na+-Ca++ exchanger. Extended presence of these two positive ions inside the myocyte prolongs the action potential and may manifest as an increased width and amplitude of the P-wave.",True,Hyper- and Hypokalemia,,,,
7fa26dd2-5ed4-410d-a9f8-67d0cd080b83,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"As hypokalemia worsens, the problems with K+ conductance and repolarization increase, and the myocardium becomes susceptible to early after-depolarization (EAD) arrhythmias.",True,Hyper- and Hypokalemia,,,,
a4be3386-8c13-4368-99ba-a5f1d2d0a06e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a4be3386-8c13-4368-99ba-a5f1d2d0a06e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a4be3386-8c13-4368-99ba-a5f1d2d0a06e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a4be3386-8c13-4368-99ba-a5f1d2d0a06e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a4be3386-8c13-4368-99ba-a5f1d2d0a06e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a4be3386-8c13-4368-99ba-a5f1d2d0a06e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a4be3386-8c13-4368-99ba-a5f1d2d0a06e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a4be3386-8c13-4368-99ba-a5f1d2d0a06e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a4be3386-8c13-4368-99ba-a5f1d2d0a06e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a4be3386-8c13-4368-99ba-a5f1d2d0a06e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a4be3386-8c13-4368-99ba-a5f1d2d0a06e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a4be3386-8c13-4368-99ba-a5f1d2d0a06e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a4be3386-8c13-4368-99ba-a5f1d2d0a06e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a4be3386-8c13-4368-99ba-a5f1d2d0a06e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a4be3386-8c13-4368-99ba-a5f1d2d0a06e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a4be3386-8c13-4368-99ba-a5f1d2d0a06e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
a4be3386-8c13-4368-99ba-a5f1d2d0a06e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
2098715c-481b-4546-9eb6-2688d23929bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2098715c-481b-4546-9eb6-2688d23929bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2098715c-481b-4546-9eb6-2688d23929bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2098715c-481b-4546-9eb6-2688d23929bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2098715c-481b-4546-9eb6-2688d23929bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2098715c-481b-4546-9eb6-2688d23929bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2098715c-481b-4546-9eb6-2688d23929bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2098715c-481b-4546-9eb6-2688d23929bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2098715c-481b-4546-9eb6-2688d23929bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2098715c-481b-4546-9eb6-2688d23929bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2098715c-481b-4546-9eb6-2688d23929bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2098715c-481b-4546-9eb6-2688d23929bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2098715c-481b-4546-9eb6-2688d23929bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2098715c-481b-4546-9eb6-2688d23929bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2098715c-481b-4546-9eb6-2688d23929bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2098715c-481b-4546-9eb6-2688d23929bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2098715c-481b-4546-9eb6-2688d23929bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
6b2aaa08-c597-4667-98d7-c5710e51780a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
6b2aaa08-c597-4667-98d7-c5710e51780a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
6b2aaa08-c597-4667-98d7-c5710e51780a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
6b2aaa08-c597-4667-98d7-c5710e51780a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
6b2aaa08-c597-4667-98d7-c5710e51780a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
6b2aaa08-c597-4667-98d7-c5710e51780a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
6b2aaa08-c597-4667-98d7-c5710e51780a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
6b2aaa08-c597-4667-98d7-c5710e51780a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
6b2aaa08-c597-4667-98d7-c5710e51780a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
6b2aaa08-c597-4667-98d7-c5710e51780a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
6b2aaa08-c597-4667-98d7-c5710e51780a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
6b2aaa08-c597-4667-98d7-c5710e51780a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
6b2aaa08-c597-4667-98d7-c5710e51780a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
6b2aaa08-c597-4667-98d7-c5710e51780a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
6b2aaa08-c597-4667-98d7-c5710e51780a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
6b2aaa08-c597-4667-98d7-c5710e51780a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
6b2aaa08-c597-4667-98d7-c5710e51780a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
d68432de-af93-4c34-a6c9-ee933d3e973f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d68432de-af93-4c34-a6c9-ee933d3e973f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d68432de-af93-4c34-a6c9-ee933d3e973f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d68432de-af93-4c34-a6c9-ee933d3e973f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d68432de-af93-4c34-a6c9-ee933d3e973f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d68432de-af93-4c34-a6c9-ee933d3e973f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d68432de-af93-4c34-a6c9-ee933d3e973f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d68432de-af93-4c34-a6c9-ee933d3e973f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d68432de-af93-4c34-a6c9-ee933d3e973f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d68432de-af93-4c34-a6c9-ee933d3e973f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d68432de-af93-4c34-a6c9-ee933d3e973f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d68432de-af93-4c34-a6c9-ee933d3e973f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d68432de-af93-4c34-a6c9-ee933d3e973f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d68432de-af93-4c34-a6c9-ee933d3e973f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d68432de-af93-4c34-a6c9-ee933d3e973f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d68432de-af93-4c34-a6c9-ee933d3e973f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
d68432de-af93-4c34-a6c9-ee933d3e973f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
89cbc8a6-5f56-464f-a4e3-0a0055941b0b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Table 1.17: Hypo- and hyperkalemia summary.,True,Hyper- and Hypokalemia,,,,
c2e5ee57-924c-4ae9-a25b-b801f61b8939,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"References, resources, and further reading",False,"References, resources, and further reading",,,,
394a4ec8-5d49-404c-8e75-c141e870fee4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,Text,False,Text,,,,
91a6b10f-c08e-40a6-85f5-9870a355f51d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Burns, Ed, and Robert Buttner. Hypercalcaemia. Lift in the Fast Lane, 2021. https://litfl.com/hypercalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
354730e2-b9b4-4e06-bc83-f05bbd697d05,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Burns, Ed, and Robert Buttner. Hypocalcaemia. Life in the Fast Lane, 2021. https://litfl.com/hypocalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
94670401-c484-410b-9582-c28bac727cd2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Buttner, Robert, and Ed Burns. Hyperkalaemia. Life in the Fast Lane. https://litfl.com/hyperkalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
bca9f9ae-43af-4adb-96bc-b4f339d49916,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Buttner, Robert, and Ed Burns. Hypokalaemia. Life in the Fast Lane, 2021. https://litfl.com/hypokalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
4cb1d2ee-086d-4428-b54d-17e698121adf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Chhabra, Lovely, Amandeep Goyal, and Michael D. Benham. Wolff Parkinson White Syndrome. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK554437/, CC BY 4.0.",True,Text,,,,
6ed34a50-bbc3-41bf-ad94-ccddd8bc28eb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Custer, Adam M., Varun S. Yelamanchili, and Sarah L. Lappin. Multifocal Atrial Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459152/, CC BY 4.0.",True,Text,,,,
e76aa2f2-1b49-4214-b102-f14d50b4a528,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Farzam, Khashayar, and John R. Richards. Premature Ventricular Contraction. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532991/, CC BY 4.0.",True,Text,,,,
f762781e-a5c8-495f-b93a-f75de14c9ecd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Foth, Christopher, Manesh Kumar Gangwani, and Heidi Alvey. Ventricular Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532954/, CC BY 4.0.",True,Text,,,,
bebf2766-0372-4275-b787-c3f367b1d9a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Hafeez, Yamama, and Shamai A. Grossman. Sinus Bradycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK493201/, CC BY 4.0.",True,Text,,,,
d433683d-91ad-423d-801a-ce6ad392a63f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Harkness, Weston T., and Mary Hicks. Right Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK507872/, CC BY 4.0.",True,Text,,,,
20523d11-d6bb-4400-8de2-4b2341f9cf85,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Heaton, Joseph, and Srikanth Yandrapalli. Premature Atrial Contractions. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK559204/, CC BY 4.0.",True,Text,,,,
00dcf624-12b6-498d-92cd-7b21b8a1fb77,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Kashou, Anthony H., Amandeep Goyal, Tran Nguyen, and Lovely Chhabra. Atrioventricular Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459147/, CC BY 4.0.",True,Text,,,,
66c74001-bf8f-4f9c-bc3c-2b539f92571a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,“Learn the Heart.” Healio. https://www.healio.com/cardiology/learn-the-heart.,True,Text,,,,
abe0f554-d169-47e0-bee3-6fba614bd284,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Ludhwani, Dipesh, Amandeep Goyal, and Mandar Jagtap. Ventricular Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK537120/, CC BY 4.0.",True,Text,,,,
7989a1b6-3d81-4d80-97fa-dc99c8d75780,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Nesheiwat, Zeid, Amandeep Goyal, and Mandar Jagtap. Atrial Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK526072/, CC BY 4.0.",True,Text,,,,
6d08af07-7bbc-42bd-8f78-6c42add5c016,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Pipilas, Daniel C., Bruce A. Koplan, and Leonard S. Lilly. “The Electrocardiogram.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 4. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
33849b58-4c72-450e-a8bc-878c8b24b863,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Rodriguez Ziccardi, Mary, Amandeep Goyal, and Christopher V. Maani. Atrial Flutter. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK540985/, CC BY 4.0.",True,Text,,,,
f40a02e1-87c4-4030-a8c1-9a54f133931f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-3,"Scherbak, Dmitriy, and Gregory J. Hicks. Left Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK482167/, CC BY 4.0.",True,Text,,,,
eac06dd8-2b73-4f5e-8065-663c9cfa9499,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,USMLE,False,USMLE,,,,
5fdbdc51-426f-4798-865c-6fe8fa8a36cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5fdbdc51-426f-4798-865c-6fe8fa8a36cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5fdbdc51-426f-4798-865c-6fe8fa8a36cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5fdbdc51-426f-4798-865c-6fe8fa8a36cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5fdbdc51-426f-4798-865c-6fe8fa8a36cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5fdbdc51-426f-4798-865c-6fe8fa8a36cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5fdbdc51-426f-4798-865c-6fe8fa8a36cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5fdbdc51-426f-4798-865c-6fe8fa8a36cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5fdbdc51-426f-4798-865c-6fe8fa8a36cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5fdbdc51-426f-4798-865c-6fe8fa8a36cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5fdbdc51-426f-4798-865c-6fe8fa8a36cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5fdbdc51-426f-4798-865c-6fe8fa8a36cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5fdbdc51-426f-4798-865c-6fe8fa8a36cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5fdbdc51-426f-4798-865c-6fe8fa8a36cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5fdbdc51-426f-4798-865c-6fe8fa8a36cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5fdbdc51-426f-4798-865c-6fe8fa8a36cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
5fdbdc51-426f-4798-865c-6fe8fa8a36cf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
68ca0423-0fc7-4028-8dbc-88db86595977,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,10q22,False,10q22,,,,
8a9ce2ad-e38a-422e-b2a2-6d00575ea9f5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,q24,False,q24,,,,
003c89f7-6740-4d8a-be59-26418436eae9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,fibrillatory,False,fibrillatory,,,,
434f9d68-a7d5-4e79-a95d-88460b3c8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
434f9d68-a7d5-4e79-a95d-88460b3c8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
434f9d68-a7d5-4e79-a95d-88460b3c8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
434f9d68-a7d5-4e79-a95d-88460b3c8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
434f9d68-a7d5-4e79-a95d-88460b3c8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
434f9d68-a7d5-4e79-a95d-88460b3c8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
434f9d68-a7d5-4e79-a95d-88460b3c8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
434f9d68-a7d5-4e79-a95d-88460b3c8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
434f9d68-a7d5-4e79-a95d-88460b3c8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
434f9d68-a7d5-4e79-a95d-88460b3c8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
434f9d68-a7d5-4e79-a95d-88460b3c8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
434f9d68-a7d5-4e79-a95d-88460b3c8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
434f9d68-a7d5-4e79-a95d-88460b3c8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
434f9d68-a7d5-4e79-a95d-88460b3c8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
434f9d68-a7d5-4e79-a95d-88460b3c8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
434f9d68-a7d5-4e79-a95d-88460b3c8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
434f9d68-a7d5-4e79-a95d-88460b3c8a8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
43d1b424-dd38-4598-807f-3f33a92b7ae1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Table 1.1: Atrial fibrillation summary.,True,fibrillatory,,,,
3724f270-5f82-45f1-95bb-116cd14f43a7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Atrial Flutter,False,Atrial Flutter,,,,
9131e210-8e16-4dfe-9c22-46d2a196bcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
9131e210-8e16-4dfe-9c22-46d2a196bcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
9131e210-8e16-4dfe-9c22-46d2a196bcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
9131e210-8e16-4dfe-9c22-46d2a196bcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
9131e210-8e16-4dfe-9c22-46d2a196bcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
9131e210-8e16-4dfe-9c22-46d2a196bcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
9131e210-8e16-4dfe-9c22-46d2a196bcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
9131e210-8e16-4dfe-9c22-46d2a196bcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
9131e210-8e16-4dfe-9c22-46d2a196bcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
9131e210-8e16-4dfe-9c22-46d2a196bcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
9131e210-8e16-4dfe-9c22-46d2a196bcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
9131e210-8e16-4dfe-9c22-46d2a196bcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
9131e210-8e16-4dfe-9c22-46d2a196bcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
9131e210-8e16-4dfe-9c22-46d2a196bcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
9131e210-8e16-4dfe-9c22-46d2a196bcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
9131e210-8e16-4dfe-9c22-46d2a196bcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
9131e210-8e16-4dfe-9c22-46d2a196bcd9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
f3b52fcb-0c14-4d31-b121-3f5245297b16,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,macroreentrant,False,macroreentrant,,,,
877fa65b-1fea-41c7-be73-34bd85e27606,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,cavotricuspid,False,cavotricuspid,,,,
79cc16cb-2bc7-4bb3-896c-02a1d716502d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"As with atrial fibrillation, the AV node’s refractory period prevents most of the P-waves from progressing to the ventricle, but commonly the AV conduction will be 2-to-1, so with an atrial rate of 300 bpm the ventricular rate will be 150 bpm. Parasympathetic stimulation or changes in AV node refractoriness can modify how many P-waves pass into the ventricle, but the the resultant rhythm is “regularly irregular.” When the heart rate is elevated, then distinguishing flutter from fibrillation becomes challenging and slowing ventricular rate pharmaceutically (adenosine) helps the flutter waves reemerge for a definitive diagnosis to be made.",True,cavotricuspid,,,,
a513234e-be7b-4381-83f5-8bfd19a7c5d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Table 1.2: Atrial flutter summary.,True,cavotricuspid,,,,
7cf7638c-e4c9-40da-9598-0d48fa19b96a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Multifocal Atrial Tachycardia,False,Multifocal Atrial Tachycardia,,,,
18cc5dc3-1daf-4bcd-b4b8-842825499176,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
18cc5dc3-1daf-4bcd-b4b8-842825499176,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
18cc5dc3-1daf-4bcd-b4b8-842825499176,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
18cc5dc3-1daf-4bcd-b4b8-842825499176,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
18cc5dc3-1daf-4bcd-b4b8-842825499176,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
18cc5dc3-1daf-4bcd-b4b8-842825499176,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
18cc5dc3-1daf-4bcd-b4b8-842825499176,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
18cc5dc3-1daf-4bcd-b4b8-842825499176,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
18cc5dc3-1daf-4bcd-b4b8-842825499176,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
18cc5dc3-1daf-4bcd-b4b8-842825499176,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
18cc5dc3-1daf-4bcd-b4b8-842825499176,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
18cc5dc3-1daf-4bcd-b4b8-842825499176,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
18cc5dc3-1daf-4bcd-b4b8-842825499176,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
18cc5dc3-1daf-4bcd-b4b8-842825499176,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
18cc5dc3-1daf-4bcd-b4b8-842825499176,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
18cc5dc3-1daf-4bcd-b4b8-842825499176,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
18cc5dc3-1daf-4bcd-b4b8-842825499176,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
f7af87db-9c63-4d49-a727-7262eda3fb77,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"MAT frequently occurs in the setting of severe lung disease and, more specifically, during an exacerbation of lung disease. This rhythm is benign, and once the underlying lung disease is treated, it should resolve.",True,Multifocal Atrial Tachycardia,,,,
376dd83d-4c42-4079-b185-836820026e1b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Table 1.3: MAT summary.,True,Multifocal Atrial Tachycardia,,,,
b2fa3f3f-29c3-4023-9d51-b64b8d253b54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Premature Atrial Contraction,False,Premature Atrial Contraction,,,,
43d883a4-202d-4bb7-b5a4-59f63fa334ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A premature atrial contraction (PAC) is generated by a depolarization instigated outside of the SA node. This produces an extra P-wave, and consequently a shortening from previous P-P intervals is seen. The aberrant P-wave also has a different morphology from a sinus P-wave because of its different anatomical origin.",True,Premature Atrial Contraction,,,,
0a88d383-9887-44d4-a589-da7d567cb7ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
0a88d383-9887-44d4-a589-da7d567cb7ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
0a88d383-9887-44d4-a589-da7d567cb7ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
0a88d383-9887-44d4-a589-da7d567cb7ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
0a88d383-9887-44d4-a589-da7d567cb7ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
0a88d383-9887-44d4-a589-da7d567cb7ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
0a88d383-9887-44d4-a589-da7d567cb7ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
0a88d383-9887-44d4-a589-da7d567cb7ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
0a88d383-9887-44d4-a589-da7d567cb7ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
0a88d383-9887-44d4-a589-da7d567cb7ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
0a88d383-9887-44d4-a589-da7d567cb7ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
0a88d383-9887-44d4-a589-da7d567cb7ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
0a88d383-9887-44d4-a589-da7d567cb7ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
0a88d383-9887-44d4-a589-da7d567cb7ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
0a88d383-9887-44d4-a589-da7d567cb7ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
0a88d383-9887-44d4-a589-da7d567cb7ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
0a88d383-9887-44d4-a589-da7d567cb7ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
04c29952-d903-4c2c-a794-be1f74c50919,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"If a PAC occurs when the AV node has not yet recovered from its refractory period, the PAC will fail to conduct to the ventricles; meaning the PAC will not be followed by a QRS complex or the ectopic P-R interval will be prolonged. The ECG will show a premature, ectopic P-wave and then no QRS complex afterward. When this occurs along with bigeminy, the ECG can appear as if there is sinus bradycardia.",True,Premature Atrial Contraction,,,,
37568a2d-313f-42e8-8a61-bb32058663e4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Table 1.4: PAC summary.,True,Premature Atrial Contraction,,,,
0b2caef0-23e8-494e-94e1-25726a9816c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Sinus Bradycardia,False,Sinus Bradycardia,,,,
12042955-777f-40a9-beec-e326f97a6e34,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Sinus bradycardia denotes a sinus rhythm below 60 bpm. Otherwise the ECG waveform is normal on an ECG with an upright P-wave in lead II preceding every QRS complex. There are many intrinsic causes associated with the heart itself, as well as extrinsic causes, some of which are listed table 1.5. Sinus bradycardia is usually asymptomatic as rates of 40–50 bpm can maintain hemodynamic stability. Rates below this can produce symptoms of fatigue, dizziness, and dyspnea on exertion.",True,Sinus Bradycardia,,,,
139b7701-d393-4d1f-a29c-dd9ee28044de,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Table 1.5: Intrinsic and extrinsic causes associated with the heart.,True,Sinus Bradycardia,,,,
30824471-eb6d-423f-8ef7-a419cc7010c7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Table 1.6: Sinus bradycardia summary.,True,Sinus Bradycardia,,,,
90f333f0-6e22-4c83-bbe4-35035f07e4ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Premature Ventricular Contractions,False,Premature Ventricular Contractions,,,,
66ebcd71-e521-4ac1-b82d-b429d18a26a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
66ebcd71-e521-4ac1-b82d-b429d18a26a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
66ebcd71-e521-4ac1-b82d-b429d18a26a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
66ebcd71-e521-4ac1-b82d-b429d18a26a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
66ebcd71-e521-4ac1-b82d-b429d18a26a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
66ebcd71-e521-4ac1-b82d-b429d18a26a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
66ebcd71-e521-4ac1-b82d-b429d18a26a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
66ebcd71-e521-4ac1-b82d-b429d18a26a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
66ebcd71-e521-4ac1-b82d-b429d18a26a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
66ebcd71-e521-4ac1-b82d-b429d18a26a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
66ebcd71-e521-4ac1-b82d-b429d18a26a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
66ebcd71-e521-4ac1-b82d-b429d18a26a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
66ebcd71-e521-4ac1-b82d-b429d18a26a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
66ebcd71-e521-4ac1-b82d-b429d18a26a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
66ebcd71-e521-4ac1-b82d-b429d18a26a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
66ebcd71-e521-4ac1-b82d-b429d18a26a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
66ebcd71-e521-4ac1-b82d-b429d18a26a8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
138ddab8-a597-49ff-8202-418fe189d418,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Table 1.7: PVC summary.,True,Premature Ventricular Contractions,,,,
64955d2d-5af6-42e6-863e-48f8531110f4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Ventricular Tachycardia,False,Ventricular Tachycardia,,,,
29158369-e533-42aa-b415-17c037af5de6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Ventricular tachycardia (VT) is caused by reentry currents being established in the ventricular myocardium or groups of ventricular myocytes that have aberrant electrical behavior. As such, VT is usually caused by underlying cardiac disease.",True,Ventricular Tachycardia,,,,
324150cf-f2d0-4210-a4b2-3a76aa9928db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Like a PVC, the aberrant depolarizations do not follow the normal conduction pathways so are wide (>120 msecs), but unlike a PVC, VT involves a ventricular rate >100 bpm. With disorganized contractility and reduced filling time, VT can lead to hemodynamic instability and severe hypotension—hence it is life threatening.",True,Ventricular Tachycardia,,,,
2b6237ea-b7df-4c49-8266-a16d6dd71107,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The QRS morphology in VT is highly variable between patients and depends on where the arrhythmia originates. Consequently there are several ways to classify VT based on duration, symptoms, QRS morphology, rate, and origin.",True,Ventricular Tachycardia,,,,
7a019ec1-e298-45bf-adb1-a25db208b599,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Sustained VT is any VT that lasts for more than 30 seconds or is symptomatic. Nonsustained VT lasts for less than 30 seconds and is asymptomatic.,True,Ventricular Tachycardia,,,,
8f66362d-b35a-4424-8e00-ad52c157ff09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
8f66362d-b35a-4424-8e00-ad52c157ff09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
8f66362d-b35a-4424-8e00-ad52c157ff09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
8f66362d-b35a-4424-8e00-ad52c157ff09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
8f66362d-b35a-4424-8e00-ad52c157ff09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
8f66362d-b35a-4424-8e00-ad52c157ff09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
8f66362d-b35a-4424-8e00-ad52c157ff09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
8f66362d-b35a-4424-8e00-ad52c157ff09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
8f66362d-b35a-4424-8e00-ad52c157ff09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
8f66362d-b35a-4424-8e00-ad52c157ff09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
8f66362d-b35a-4424-8e00-ad52c157ff09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
8f66362d-b35a-4424-8e00-ad52c157ff09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
8f66362d-b35a-4424-8e00-ad52c157ff09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
8f66362d-b35a-4424-8e00-ad52c157ff09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
8f66362d-b35a-4424-8e00-ad52c157ff09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
8f66362d-b35a-4424-8e00-ad52c157ff09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
8f66362d-b35a-4424-8e00-ad52c157ff09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
d3aa39b8-db52-4b55-9e6a-46cb1765f900,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
d3aa39b8-db52-4b55-9e6a-46cb1765f900,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
d3aa39b8-db52-4b55-9e6a-46cb1765f900,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
d3aa39b8-db52-4b55-9e6a-46cb1765f900,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
d3aa39b8-db52-4b55-9e6a-46cb1765f900,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
d3aa39b8-db52-4b55-9e6a-46cb1765f900,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
d3aa39b8-db52-4b55-9e6a-46cb1765f900,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
d3aa39b8-db52-4b55-9e6a-46cb1765f900,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
d3aa39b8-db52-4b55-9e6a-46cb1765f900,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
d3aa39b8-db52-4b55-9e6a-46cb1765f900,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
d3aa39b8-db52-4b55-9e6a-46cb1765f900,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
d3aa39b8-db52-4b55-9e6a-46cb1765f900,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
d3aa39b8-db52-4b55-9e6a-46cb1765f900,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
d3aa39b8-db52-4b55-9e6a-46cb1765f900,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
d3aa39b8-db52-4b55-9e6a-46cb1765f900,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
d3aa39b8-db52-4b55-9e6a-46cb1765f900,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
d3aa39b8-db52-4b55-9e6a-46cb1765f900,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
950a7268-4a94-4ad4-8c0a-7c1c0a3ece0d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Torsades de pointes is associated with a prolonged QT interval (>600 msecs) that helps distinguish it from other forms of polymorphous VT. The longer QT interval can be caused by ionic abnormalities that reduce the repolarizing current of Phase 3 of the cardiac action potential. This makes the myocardium susceptible to early after-depolarizations—the trigger for torsades de pointes. These after-depolarizations do not happen uniformly across the myocardium and are more common in endocardial tissue where the repolarization currents are slower. So torsades de pointes arises from the after-depolarizations causing reentry currents in neighboring tissue.,True,Ventricular Tachycardia,,,,
2e2e0ad3-d267-429f-946b-3e0ca0a898c6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Both common garden variety VTs and torsades de pointes can progress to ventricular fibrillation.,True,Ventricular Tachycardia,,,,
642bfce3-8318-4532-8ecc-03eb61f666cb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Table 1.8: VT summary.,True,Ventricular Tachycardia,,,,
63e2a130-c6ed-493f-8003-1ab154c18f84,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Ventricular Fibrillation,False,Ventricular Fibrillation,,,,
f44bd700-0ca9-4000-b728-4130de102f70,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Ventricular fibrillation (VF) occurs when the ventricular rate exceeds 400 bpm. The disorganized and uncoordinated contraction of the myocardium causes cardiac output to fall to catastrophic levels. Rates of survival for out-of-hospital VF are low.,True,Ventricular Fibrillation,,,,
d607f1d2-32a4-4dfa-ab62-5f73d1b6fdee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
d607f1d2-32a4-4dfa-ab62-5f73d1b6fdee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
d607f1d2-32a4-4dfa-ab62-5f73d1b6fdee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
d607f1d2-32a4-4dfa-ab62-5f73d1b6fdee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
d607f1d2-32a4-4dfa-ab62-5f73d1b6fdee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
d607f1d2-32a4-4dfa-ab62-5f73d1b6fdee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
d607f1d2-32a4-4dfa-ab62-5f73d1b6fdee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
d607f1d2-32a4-4dfa-ab62-5f73d1b6fdee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
d607f1d2-32a4-4dfa-ab62-5f73d1b6fdee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
d607f1d2-32a4-4dfa-ab62-5f73d1b6fdee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
d607f1d2-32a4-4dfa-ab62-5f73d1b6fdee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
d607f1d2-32a4-4dfa-ab62-5f73d1b6fdee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
d607f1d2-32a4-4dfa-ab62-5f73d1b6fdee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
d607f1d2-32a4-4dfa-ab62-5f73d1b6fdee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
d607f1d2-32a4-4dfa-ab62-5f73d1b6fdee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
d607f1d2-32a4-4dfa-ab62-5f73d1b6fdee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
d607f1d2-32a4-4dfa-ab62-5f73d1b6fdee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
6e6aa36f-0a96-48d6-887c-1a65d1e9fe33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Table 1.9: VF summary.,True,Ventricular Fibrillation,,,,
5550ea75-3166-4202-b80c-98c1fed7fec6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,First-Degree Atrioventricular Block,False,First-Degree Atrioventricular Block,,,,
354e71bb-bd4e-44fd-9ebd-731e602d0638,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
354e71bb-bd4e-44fd-9ebd-731e602d0638,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
354e71bb-bd4e-44fd-9ebd-731e602d0638,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
354e71bb-bd4e-44fd-9ebd-731e602d0638,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
354e71bb-bd4e-44fd-9ebd-731e602d0638,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
354e71bb-bd4e-44fd-9ebd-731e602d0638,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
354e71bb-bd4e-44fd-9ebd-731e602d0638,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
354e71bb-bd4e-44fd-9ebd-731e602d0638,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
354e71bb-bd4e-44fd-9ebd-731e602d0638,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
354e71bb-bd4e-44fd-9ebd-731e602d0638,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
354e71bb-bd4e-44fd-9ebd-731e602d0638,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
354e71bb-bd4e-44fd-9ebd-731e602d0638,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
354e71bb-bd4e-44fd-9ebd-731e602d0638,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
354e71bb-bd4e-44fd-9ebd-731e602d0638,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
354e71bb-bd4e-44fd-9ebd-731e602d0638,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
354e71bb-bd4e-44fd-9ebd-731e602d0638,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
354e71bb-bd4e-44fd-9ebd-731e602d0638,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f1c2f4b3-f60d-4d13-a42d-af3867d126f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f1c2f4b3-f60d-4d13-a42d-af3867d126f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f1c2f4b3-f60d-4d13-a42d-af3867d126f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f1c2f4b3-f60d-4d13-a42d-af3867d126f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f1c2f4b3-f60d-4d13-a42d-af3867d126f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f1c2f4b3-f60d-4d13-a42d-af3867d126f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f1c2f4b3-f60d-4d13-a42d-af3867d126f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f1c2f4b3-f60d-4d13-a42d-af3867d126f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f1c2f4b3-f60d-4d13-a42d-af3867d126f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f1c2f4b3-f60d-4d13-a42d-af3867d126f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f1c2f4b3-f60d-4d13-a42d-af3867d126f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f1c2f4b3-f60d-4d13-a42d-af3867d126f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f1c2f4b3-f60d-4d13-a42d-af3867d126f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f1c2f4b3-f60d-4d13-a42d-af3867d126f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f1c2f4b3-f60d-4d13-a42d-af3867d126f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f1c2f4b3-f60d-4d13-a42d-af3867d126f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f1c2f4b3-f60d-4d13-a42d-af3867d126f6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
d5d50ade-c2fa-478b-8a54-7f85772be77a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Table 1.10: First-degree block summary.,True,First-Degree Atrioventricular Block,,,,
022277a8-0348-4718-bfab-19615d479e86,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Second-Degree Atrioventricular Block,False,Second-Degree Atrioventricular Block,,,,
d0ae3f14-fe6f-4ce3-aba7-e1d2427bdae5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A second-degree atrioventricular block also has changes in P-R interval, but it starts to show failure of the P-wave to propagate a QRS complex every time (i.e., intermittently the depolarization fails to reach the ventricles). The pattern of missed ventricular depolarizations, or blocked P-waves, is often very regular and described as a ratio of P-waves to QRS complex. The way in which the P-R interval changes in relation to the blocked P-waves produces subclassifications of second-degree blocks, Mobitz I and II.",True,Second-Degree Atrioventricular Block,,,,
9cca533b-9b37-4202-b5c0-4fd149d454c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9cca533b-9b37-4202-b5c0-4fd149d454c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9cca533b-9b37-4202-b5c0-4fd149d454c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9cca533b-9b37-4202-b5c0-4fd149d454c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9cca533b-9b37-4202-b5c0-4fd149d454c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9cca533b-9b37-4202-b5c0-4fd149d454c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9cca533b-9b37-4202-b5c0-4fd149d454c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9cca533b-9b37-4202-b5c0-4fd149d454c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9cca533b-9b37-4202-b5c0-4fd149d454c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9cca533b-9b37-4202-b5c0-4fd149d454c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9cca533b-9b37-4202-b5c0-4fd149d454c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9cca533b-9b37-4202-b5c0-4fd149d454c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9cca533b-9b37-4202-b5c0-4fd149d454c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9cca533b-9b37-4202-b5c0-4fd149d454c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9cca533b-9b37-4202-b5c0-4fd149d454c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9cca533b-9b37-4202-b5c0-4fd149d454c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9cca533b-9b37-4202-b5c0-4fd149d454c0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
a0c659d0-a003-4dd2-8b9f-b2081dd9f968,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a0c659d0-a003-4dd2-8b9f-b2081dd9f968,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a0c659d0-a003-4dd2-8b9f-b2081dd9f968,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a0c659d0-a003-4dd2-8b9f-b2081dd9f968,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a0c659d0-a003-4dd2-8b9f-b2081dd9f968,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a0c659d0-a003-4dd2-8b9f-b2081dd9f968,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a0c659d0-a003-4dd2-8b9f-b2081dd9f968,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a0c659d0-a003-4dd2-8b9f-b2081dd9f968,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a0c659d0-a003-4dd2-8b9f-b2081dd9f968,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a0c659d0-a003-4dd2-8b9f-b2081dd9f968,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a0c659d0-a003-4dd2-8b9f-b2081dd9f968,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a0c659d0-a003-4dd2-8b9f-b2081dd9f968,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a0c659d0-a003-4dd2-8b9f-b2081dd9f968,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a0c659d0-a003-4dd2-8b9f-b2081dd9f968,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a0c659d0-a003-4dd2-8b9f-b2081dd9f968,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a0c659d0-a003-4dd2-8b9f-b2081dd9f968,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
a0c659d0-a003-4dd2-8b9f-b2081dd9f968,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
8a483554-00c4-4c73-b93e-261e798a25d5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Table 1.11: Second-degree block summary.,True,Second-Degree Atrioventricular Block,,,,
3f562aee-20ca-4eff-97d2-0394fb01af07,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Third-Degree Atrioventricular Block,False,Third-Degree Atrioventricular Block,,,,
b3ba1c68-5603-4d3e-b4c1-b37d4c9f2de0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b3ba1c68-5603-4d3e-b4c1-b37d4c9f2de0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b3ba1c68-5603-4d3e-b4c1-b37d4c9f2de0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b3ba1c68-5603-4d3e-b4c1-b37d4c9f2de0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b3ba1c68-5603-4d3e-b4c1-b37d4c9f2de0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b3ba1c68-5603-4d3e-b4c1-b37d4c9f2de0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b3ba1c68-5603-4d3e-b4c1-b37d4c9f2de0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b3ba1c68-5603-4d3e-b4c1-b37d4c9f2de0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b3ba1c68-5603-4d3e-b4c1-b37d4c9f2de0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b3ba1c68-5603-4d3e-b4c1-b37d4c9f2de0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b3ba1c68-5603-4d3e-b4c1-b37d4c9f2de0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b3ba1c68-5603-4d3e-b4c1-b37d4c9f2de0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b3ba1c68-5603-4d3e-b4c1-b37d4c9f2de0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b3ba1c68-5603-4d3e-b4c1-b37d4c9f2de0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b3ba1c68-5603-4d3e-b4c1-b37d4c9f2de0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b3ba1c68-5603-4d3e-b4c1-b37d4c9f2de0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
b3ba1c68-5603-4d3e-b4c1-b37d4c9f2de0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
17057db3-bfc5-4c73-82a4-e87aa1354c53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Table 1.12: Third-degree block summary.,True,Third-Degree Atrioventricular Block,,,,
1f4c19a4-a2e2-4ff8-b3cb-8412758c4fa9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Left Bundle Branch Block,False,Left Bundle Branch Block,,,,
3d930be0-3022-46f3-bb79-7ca954b37d16,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"A left bundle branch block (LBBB) is generated when the conductivity of the His-Purkinje system in the left ventricle is compromised, either through damage or disease. The ECG changes, and criteria for LBBB relate to these changes in conductivity and the left-side location.",True,Left Bundle Branch Block,,,,
b7f9ddf7-3d02-4489-9dc3-122ff9b42dae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b7f9ddf7-3d02-4489-9dc3-122ff9b42dae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b7f9ddf7-3d02-4489-9dc3-122ff9b42dae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b7f9ddf7-3d02-4489-9dc3-122ff9b42dae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b7f9ddf7-3d02-4489-9dc3-122ff9b42dae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b7f9ddf7-3d02-4489-9dc3-122ff9b42dae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b7f9ddf7-3d02-4489-9dc3-122ff9b42dae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b7f9ddf7-3d02-4489-9dc3-122ff9b42dae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b7f9ddf7-3d02-4489-9dc3-122ff9b42dae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b7f9ddf7-3d02-4489-9dc3-122ff9b42dae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b7f9ddf7-3d02-4489-9dc3-122ff9b42dae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b7f9ddf7-3d02-4489-9dc3-122ff9b42dae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b7f9ddf7-3d02-4489-9dc3-122ff9b42dae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b7f9ddf7-3d02-4489-9dc3-122ff9b42dae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b7f9ddf7-3d02-4489-9dc3-122ff9b42dae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b7f9ddf7-3d02-4489-9dc3-122ff9b42dae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
b7f9ddf7-3d02-4489-9dc3-122ff9b42dae,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
bc14256d-f97b-4a5e-a892-82b99ce70346,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The lateral leads (I, V5, and V6) normally show a downward deflecting Q-wave as normal septal deflection initially occurs left-to-right (i.e., away from the lateral leads). In LBBB the change in direction to right-to-left, plus the longer duration, eliminates the Q-wave from the lateral leads, and Q-waves will be small in aVL.",True,Left Bundle Branch Block,,,,
e6c1ffaa-53c5-4711-9659-0ed8cde643af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
e6c1ffaa-53c5-4711-9659-0ed8cde643af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
e6c1ffaa-53c5-4711-9659-0ed8cde643af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
e6c1ffaa-53c5-4711-9659-0ed8cde643af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
e6c1ffaa-53c5-4711-9659-0ed8cde643af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
e6c1ffaa-53c5-4711-9659-0ed8cde643af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
e6c1ffaa-53c5-4711-9659-0ed8cde643af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
e6c1ffaa-53c5-4711-9659-0ed8cde643af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
e6c1ffaa-53c5-4711-9659-0ed8cde643af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
e6c1ffaa-53c5-4711-9659-0ed8cde643af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
e6c1ffaa-53c5-4711-9659-0ed8cde643af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
e6c1ffaa-53c5-4711-9659-0ed8cde643af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
e6c1ffaa-53c5-4711-9659-0ed8cde643af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
e6c1ffaa-53c5-4711-9659-0ed8cde643af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
e6c1ffaa-53c5-4711-9659-0ed8cde643af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
e6c1ffaa-53c5-4711-9659-0ed8cde643af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
e6c1ffaa-53c5-4711-9659-0ed8cde643af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
65ca9ec0-5002-4906-947f-e4c336c10a7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
65ca9ec0-5002-4906-947f-e4c336c10a7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
65ca9ec0-5002-4906-947f-e4c336c10a7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
65ca9ec0-5002-4906-947f-e4c336c10a7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
65ca9ec0-5002-4906-947f-e4c336c10a7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
65ca9ec0-5002-4906-947f-e4c336c10a7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
65ca9ec0-5002-4906-947f-e4c336c10a7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
65ca9ec0-5002-4906-947f-e4c336c10a7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
65ca9ec0-5002-4906-947f-e4c336c10a7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
65ca9ec0-5002-4906-947f-e4c336c10a7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
65ca9ec0-5002-4906-947f-e4c336c10a7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
65ca9ec0-5002-4906-947f-e4c336c10a7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
65ca9ec0-5002-4906-947f-e4c336c10a7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
65ca9ec0-5002-4906-947f-e4c336c10a7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
65ca9ec0-5002-4906-947f-e4c336c10a7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
65ca9ec0-5002-4906-947f-e4c336c10a7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
65ca9ec0-5002-4906-947f-e4c336c10a7a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
64a9285c-c0ef-467e-8dbe-f4f6cec791f2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Table 1.13: LBBB summary.,True,Left Bundle Branch Block,,,,
53bdb438-ed38-49c7-8772-f92b31491e24,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Right Bundle Branch Block,False,Right Bundle Branch Block,,,,
14259858-402f-4059-8787-1bc727837b3e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The causes and manifestations of a right bundle branch block (RBBB) bear some similarities to those described for LBBB, but of course this time its depolarization of the right ventricle is delayed. Causes of RBBB include ischemic heart disease again as well as other myocardial diseases, but pulmonary issues such as pulmonary embolism and cor pulmonale can be added to the list.",True,Right Bundle Branch Block,,,,
354cbe38-57ff-46ba-a72d-90ea60476747,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
354cbe38-57ff-46ba-a72d-90ea60476747,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
354cbe38-57ff-46ba-a72d-90ea60476747,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
354cbe38-57ff-46ba-a72d-90ea60476747,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
354cbe38-57ff-46ba-a72d-90ea60476747,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
354cbe38-57ff-46ba-a72d-90ea60476747,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
354cbe38-57ff-46ba-a72d-90ea60476747,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
354cbe38-57ff-46ba-a72d-90ea60476747,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
354cbe38-57ff-46ba-a72d-90ea60476747,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
354cbe38-57ff-46ba-a72d-90ea60476747,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
354cbe38-57ff-46ba-a72d-90ea60476747,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
354cbe38-57ff-46ba-a72d-90ea60476747,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
354cbe38-57ff-46ba-a72d-90ea60476747,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
354cbe38-57ff-46ba-a72d-90ea60476747,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
354cbe38-57ff-46ba-a72d-90ea60476747,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
354cbe38-57ff-46ba-a72d-90ea60476747,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
354cbe38-57ff-46ba-a72d-90ea60476747,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
088483ff-c14c-4664-8823-b59dd959f869,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Table 1.14: RBBB summary.,True,Right Bundle Branch Block,,,,
7a656429-2086-4f1a-926b-768a029114b6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Wolff-Parkinson-White Syndrome,False,Wolff-Parkinson-White Syndrome,,,,
4cd3b604-a493-4c2f-b28d-919f8664766b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Normally the only electrical connection between the atria and the ventricles is the AV node. Otherwise the fibrous skeleton of the heart electrically insulates the atria from the ventricles. In Wolff-Parkinson-White (WPW) syndrome, that insulation is incomplete, and an “accessory pathway” connects the electrical system of the atria directly to the ventricles. If you think of the AV node as a bridge over the fibrous wall with regulated access, the accessory pathway is like a pathological tunnel under it with no regulation.",True,Wolff-Parkinson-White Syndrome,,,,
62b473c5-f856-4657-8721-310de1a23c52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
62b473c5-f856-4657-8721-310de1a23c52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
62b473c5-f856-4657-8721-310de1a23c52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
62b473c5-f856-4657-8721-310de1a23c52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
62b473c5-f856-4657-8721-310de1a23c52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
62b473c5-f856-4657-8721-310de1a23c52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
62b473c5-f856-4657-8721-310de1a23c52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
62b473c5-f856-4657-8721-310de1a23c52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
62b473c5-f856-4657-8721-310de1a23c52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
62b473c5-f856-4657-8721-310de1a23c52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
62b473c5-f856-4657-8721-310de1a23c52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
62b473c5-f856-4657-8721-310de1a23c52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
62b473c5-f856-4657-8721-310de1a23c52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
62b473c5-f856-4657-8721-310de1a23c52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
62b473c5-f856-4657-8721-310de1a23c52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
62b473c5-f856-4657-8721-310de1a23c52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
62b473c5-f856-4657-8721-310de1a23c52,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
638ad552-5d1b-42fa-a4dc-18df51020f4c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"WPW syndrome is often asymptomatic, and patients do not require immediate treatment. However, if atrial fibrillation occurs in a WPW patient, the accessory pathway can allow the atrial fibrillation waves through to the ventricle (with no AV nodal refractory period to prevent them). Consequently a high ventricular rate is seen, and the risk of ventricular fibrillation being established means immediate clinical attention is required.",True,Wolff-Parkinson-White Syndrome,,,,
85e929cb-e390-45da-a542-673f31355554,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Hyper- and Hypocalcemia,False,Hyper- and Hypocalcemia,,,,
e9023b6d-1436-4996-bc79-2baf8a816600,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e9023b6d-1436-4996-bc79-2baf8a816600,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e9023b6d-1436-4996-bc79-2baf8a816600,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e9023b6d-1436-4996-bc79-2baf8a816600,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e9023b6d-1436-4996-bc79-2baf8a816600,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e9023b6d-1436-4996-bc79-2baf8a816600,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e9023b6d-1436-4996-bc79-2baf8a816600,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e9023b6d-1436-4996-bc79-2baf8a816600,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e9023b6d-1436-4996-bc79-2baf8a816600,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e9023b6d-1436-4996-bc79-2baf8a816600,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e9023b6d-1436-4996-bc79-2baf8a816600,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e9023b6d-1436-4996-bc79-2baf8a816600,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e9023b6d-1436-4996-bc79-2baf8a816600,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e9023b6d-1436-4996-bc79-2baf8a816600,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e9023b6d-1436-4996-bc79-2baf8a816600,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e9023b6d-1436-4996-bc79-2baf8a816600,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
e9023b6d-1436-4996-bc79-2baf8a816600,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
b3cd6c2d-66df-4e7d-84cd-6818a665f0b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
b3cd6c2d-66df-4e7d-84cd-6818a665f0b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
b3cd6c2d-66df-4e7d-84cd-6818a665f0b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
b3cd6c2d-66df-4e7d-84cd-6818a665f0b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
b3cd6c2d-66df-4e7d-84cd-6818a665f0b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
b3cd6c2d-66df-4e7d-84cd-6818a665f0b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
b3cd6c2d-66df-4e7d-84cd-6818a665f0b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
b3cd6c2d-66df-4e7d-84cd-6818a665f0b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
b3cd6c2d-66df-4e7d-84cd-6818a665f0b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
b3cd6c2d-66df-4e7d-84cd-6818a665f0b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
b3cd6c2d-66df-4e7d-84cd-6818a665f0b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
b3cd6c2d-66df-4e7d-84cd-6818a665f0b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
b3cd6c2d-66df-4e7d-84cd-6818a665f0b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
b3cd6c2d-66df-4e7d-84cd-6818a665f0b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
b3cd6c2d-66df-4e7d-84cd-6818a665f0b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
b3cd6c2d-66df-4e7d-84cd-6818a665f0b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
b3cd6c2d-66df-4e7d-84cd-6818a665f0b1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
b8c91456-d9c9-4665-948f-7750d9045ba6,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Table 1.16: Hyper- and hypocalcemia summary.,True,Hyper- and Hypocalcemia,,,,
48ac23c0-d85e-4163-a331-8e00c1e66249,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Hyper- and Hypokalemia,False,Hyper- and Hypokalemia,,,,
f0f6329c-76e8-4af2-a3ab-5934b9522549,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"The pathophysiology is not as simple as changes in extracellular K+ changing the electrochemical gradient for K+. Because of potassium’s role in maintaining the resting membrane potential, shifts in extracellular potassium can also influence the activity of Na+ and Ca++ channels.",True,Hyper- and Hypokalemia,,,,
32343fd5-833f-4318-b2c0-731a3e6b0a27,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
32343fd5-833f-4318-b2c0-731a3e6b0a27,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
32343fd5-833f-4318-b2c0-731a3e6b0a27,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
32343fd5-833f-4318-b2c0-731a3e6b0a27,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
32343fd5-833f-4318-b2c0-731a3e6b0a27,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
32343fd5-833f-4318-b2c0-731a3e6b0a27,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
32343fd5-833f-4318-b2c0-731a3e6b0a27,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
32343fd5-833f-4318-b2c0-731a3e6b0a27,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
32343fd5-833f-4318-b2c0-731a3e6b0a27,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
32343fd5-833f-4318-b2c0-731a3e6b0a27,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
32343fd5-833f-4318-b2c0-731a3e6b0a27,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
32343fd5-833f-4318-b2c0-731a3e6b0a27,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
32343fd5-833f-4318-b2c0-731a3e6b0a27,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
32343fd5-833f-4318-b2c0-731a3e6b0a27,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
32343fd5-833f-4318-b2c0-731a3e6b0a27,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
32343fd5-833f-4318-b2c0-731a3e6b0a27,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
32343fd5-833f-4318-b2c0-731a3e6b0a27,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
438718e2-fa8d-4ea8-bcab-1df0a8eefa9f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"As hypokalemia also inhibits Na+-K+ ATPase, Na+ accumulates inside the cell. This in turn leads to an accumulation of Ca++ because of a subsequent failure of the Na+-Ca++ exchanger. Extended presence of these two positive ions inside the myocyte prolongs the action potential and may manifest as an increased width and amplitude of the P-wave.",True,Hyper- and Hypokalemia,,,,
4aa30e96-1bc3-4d72-8ec2-393ba71b2c92,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"As hypokalemia worsens, the problems with K+ conductance and repolarization increase, and the myocardium becomes susceptible to early after-depolarization (EAD) arrhythmias.",True,Hyper- and Hypokalemia,,,,
fb425aba-7ad8-4ddf-b034-4e8e7744279e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fb425aba-7ad8-4ddf-b034-4e8e7744279e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fb425aba-7ad8-4ddf-b034-4e8e7744279e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fb425aba-7ad8-4ddf-b034-4e8e7744279e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fb425aba-7ad8-4ddf-b034-4e8e7744279e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fb425aba-7ad8-4ddf-b034-4e8e7744279e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fb425aba-7ad8-4ddf-b034-4e8e7744279e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fb425aba-7ad8-4ddf-b034-4e8e7744279e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fb425aba-7ad8-4ddf-b034-4e8e7744279e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fb425aba-7ad8-4ddf-b034-4e8e7744279e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fb425aba-7ad8-4ddf-b034-4e8e7744279e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fb425aba-7ad8-4ddf-b034-4e8e7744279e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fb425aba-7ad8-4ddf-b034-4e8e7744279e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fb425aba-7ad8-4ddf-b034-4e8e7744279e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fb425aba-7ad8-4ddf-b034-4e8e7744279e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fb425aba-7ad8-4ddf-b034-4e8e7744279e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
fb425aba-7ad8-4ddf-b034-4e8e7744279e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
1e1ab226-4e15-42d0-827b-7be3fb9cef64,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
1e1ab226-4e15-42d0-827b-7be3fb9cef64,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
1e1ab226-4e15-42d0-827b-7be3fb9cef64,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
1e1ab226-4e15-42d0-827b-7be3fb9cef64,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
1e1ab226-4e15-42d0-827b-7be3fb9cef64,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
1e1ab226-4e15-42d0-827b-7be3fb9cef64,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
1e1ab226-4e15-42d0-827b-7be3fb9cef64,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
1e1ab226-4e15-42d0-827b-7be3fb9cef64,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
1e1ab226-4e15-42d0-827b-7be3fb9cef64,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
1e1ab226-4e15-42d0-827b-7be3fb9cef64,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
1e1ab226-4e15-42d0-827b-7be3fb9cef64,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
1e1ab226-4e15-42d0-827b-7be3fb9cef64,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
1e1ab226-4e15-42d0-827b-7be3fb9cef64,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
1e1ab226-4e15-42d0-827b-7be3fb9cef64,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
1e1ab226-4e15-42d0-827b-7be3fb9cef64,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
1e1ab226-4e15-42d0-827b-7be3fb9cef64,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
1e1ab226-4e15-42d0-827b-7be3fb9cef64,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
da5e9e38-00cf-49c4-b4c2-87a27a66bcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
da5e9e38-00cf-49c4-b4c2-87a27a66bcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
da5e9e38-00cf-49c4-b4c2-87a27a66bcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
da5e9e38-00cf-49c4-b4c2-87a27a66bcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
da5e9e38-00cf-49c4-b4c2-87a27a66bcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
da5e9e38-00cf-49c4-b4c2-87a27a66bcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
da5e9e38-00cf-49c4-b4c2-87a27a66bcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
da5e9e38-00cf-49c4-b4c2-87a27a66bcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
da5e9e38-00cf-49c4-b4c2-87a27a66bcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
da5e9e38-00cf-49c4-b4c2-87a27a66bcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
da5e9e38-00cf-49c4-b4c2-87a27a66bcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
da5e9e38-00cf-49c4-b4c2-87a27a66bcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
da5e9e38-00cf-49c4-b4c2-87a27a66bcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
da5e9e38-00cf-49c4-b4c2-87a27a66bcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
da5e9e38-00cf-49c4-b4c2-87a27a66bcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
da5e9e38-00cf-49c4-b4c2-87a27a66bcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
da5e9e38-00cf-49c4-b4c2-87a27a66bcea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
1e38bd78-5b49-4f01-9498-9fff8a674b41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
1e38bd78-5b49-4f01-9498-9fff8a674b41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
1e38bd78-5b49-4f01-9498-9fff8a674b41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
1e38bd78-5b49-4f01-9498-9fff8a674b41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
1e38bd78-5b49-4f01-9498-9fff8a674b41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
1e38bd78-5b49-4f01-9498-9fff8a674b41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
1e38bd78-5b49-4f01-9498-9fff8a674b41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
1e38bd78-5b49-4f01-9498-9fff8a674b41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
1e38bd78-5b49-4f01-9498-9fff8a674b41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
1e38bd78-5b49-4f01-9498-9fff8a674b41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
1e38bd78-5b49-4f01-9498-9fff8a674b41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
1e38bd78-5b49-4f01-9498-9fff8a674b41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
1e38bd78-5b49-4f01-9498-9fff8a674b41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
1e38bd78-5b49-4f01-9498-9fff8a674b41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
1e38bd78-5b49-4f01-9498-9fff8a674b41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
1e38bd78-5b49-4f01-9498-9fff8a674b41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
1e38bd78-5b49-4f01-9498-9fff8a674b41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
320b25aa-a6a9-40ad-912c-e6297b3710cd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Table 1.17: Hypo- and hyperkalemia summary.,True,Hyper- and Hypokalemia,,,,
e51c3e8b-ccf4-41a4-94f8-677d81621403,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"References, resources, and further reading",False,"References, resources, and further reading",,,,
9ae89e4c-9830-4f9f-a2de-dfd9b3019e5b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,Text,False,Text,,,,
96d05128-f4b2-4c54-a0e2-a2a29db85f38,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Burns, Ed, and Robert Buttner. Hypercalcaemia. Lift in the Fast Lane, 2021. https://litfl.com/hypercalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
bde20e2a-641c-47be-b7cf-a91fab312f24,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Burns, Ed, and Robert Buttner. Hypocalcaemia. Life in the Fast Lane, 2021. https://litfl.com/hypocalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
d756f5bc-0c7c-453f-b498-535b89e9f535,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Buttner, Robert, and Ed Burns. Hyperkalaemia. Life in the Fast Lane. https://litfl.com/hyperkalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
a90da919-38ed-4d5d-a7b7-0ddfcd970d04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Buttner, Robert, and Ed Burns. Hypokalaemia. Life in the Fast Lane, 2021. https://litfl.com/hypokalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
d8fe48db-a8fa-4e51-a7d0-38e6f86ddd48,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Chhabra, Lovely, Amandeep Goyal, and Michael D. Benham. Wolff Parkinson White Syndrome. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK554437/, CC BY 4.0.",True,Text,,,,
14d3f7d0-2965-4313-bab9-7c6788a928d2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Custer, Adam M., Varun S. Yelamanchili, and Sarah L. Lappin. Multifocal Atrial Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459152/, CC BY 4.0.",True,Text,,,,
429ed38e-0106-4e6e-a841-6e424de21ea3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Farzam, Khashayar, and John R. Richards. Premature Ventricular Contraction. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532991/, CC BY 4.0.",True,Text,,,,
9538d0c5-b14b-4d41-9407-1b550beca497,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Foth, Christopher, Manesh Kumar Gangwani, and Heidi Alvey. Ventricular Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532954/, CC BY 4.0.",True,Text,,,,
c28a16f3-fdd3-4527-855c-76be80fc675d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Hafeez, Yamama, and Shamai A. Grossman. Sinus Bradycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK493201/, CC BY 4.0.",True,Text,,,,
a10b6365-0e05-4311-9a08-c0fd09ead23b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Harkness, Weston T., and Mary Hicks. Right Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK507872/, CC BY 4.0.",True,Text,,,,
9ae78289-3962-41cf-afec-2aa277b6ea2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Heaton, Joseph, and Srikanth Yandrapalli. Premature Atrial Contractions. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK559204/, CC BY 4.0.",True,Text,,,,
7457d966-35ab-4ad5-a656-43f426212aea,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Kashou, Anthony H., Amandeep Goyal, Tran Nguyen, and Lovely Chhabra. Atrioventricular Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459147/, CC BY 4.0.",True,Text,,,,
ba0ea1ce-3247-45cf-9d22-ec0ceb795174,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,“Learn the Heart.” Healio. https://www.healio.com/cardiology/learn-the-heart.,True,Text,,,,
dc23267b-fe8d-4dff-980f-64d0e25332e9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Ludhwani, Dipesh, Amandeep Goyal, and Mandar Jagtap. Ventricular Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK537120/, CC BY 4.0.",True,Text,,,,
2c55b298-6c1e-4292-a761-9040bd016464,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Nesheiwat, Zeid, Amandeep Goyal, and Mandar Jagtap. Atrial Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK526072/, CC BY 4.0.",True,Text,,,,
cb495e97-318c-4b95-b623-827c91af8a2d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Pipilas, Daniel C., Bruce A. Koplan, and Leonard S. Lilly. “The Electrocardiogram.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 4. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
69e77b83-4b7a-46af-bda3-8e4a849eaa53,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Rodriguez Ziccardi, Mary, Amandeep Goyal, and Christopher V. Maani. Atrial Flutter. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK540985/, CC BY 4.0.",True,Text,,,,
7c394b1d-35a6-4633-8e51-bf8b02becab2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Flutter,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-2,"Scherbak, Dmitriy, and Gregory J. Hicks. Left Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK482167/, CC BY 4.0.",True,Text,,,,
b0f4ecfe-853b-4aaf-8b83-5321684508e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,USMLE,False,USMLE,,,,
7d78e8f5-ea46-46da-b5fa-fb039e7cd8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
7d78e8f5-ea46-46da-b5fa-fb039e7cd8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
7d78e8f5-ea46-46da-b5fa-fb039e7cd8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
7d78e8f5-ea46-46da-b5fa-fb039e7cd8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
7d78e8f5-ea46-46da-b5fa-fb039e7cd8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
7d78e8f5-ea46-46da-b5fa-fb039e7cd8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
7d78e8f5-ea46-46da-b5fa-fb039e7cd8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
7d78e8f5-ea46-46da-b5fa-fb039e7cd8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
7d78e8f5-ea46-46da-b5fa-fb039e7cd8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
7d78e8f5-ea46-46da-b5fa-fb039e7cd8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
7d78e8f5-ea46-46da-b5fa-fb039e7cd8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
7d78e8f5-ea46-46da-b5fa-fb039e7cd8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
7d78e8f5-ea46-46da-b5fa-fb039e7cd8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
7d78e8f5-ea46-46da-b5fa-fb039e7cd8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
7d78e8f5-ea46-46da-b5fa-fb039e7cd8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
7d78e8f5-ea46-46da-b5fa-fb039e7cd8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
7d78e8f5-ea46-46da-b5fa-fb039e7cd8c2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
1a82f431-05bd-4bb9-be8b-9a4644c4ce24,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,10q22,False,10q22,,,,
8c3e486e-7be2-4a16-bbfc-cfd980f70a91,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,q24,False,q24,,,,
0ad05582-a338-4fdb-a76c-d23090fff91d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,fibrillatory,False,fibrillatory,,,,
21275a38-5e09-44e5-9d4b-267b408a49c9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
21275a38-5e09-44e5-9d4b-267b408a49c9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
21275a38-5e09-44e5-9d4b-267b408a49c9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
21275a38-5e09-44e5-9d4b-267b408a49c9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
21275a38-5e09-44e5-9d4b-267b408a49c9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
21275a38-5e09-44e5-9d4b-267b408a49c9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
21275a38-5e09-44e5-9d4b-267b408a49c9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
21275a38-5e09-44e5-9d4b-267b408a49c9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
21275a38-5e09-44e5-9d4b-267b408a49c9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
21275a38-5e09-44e5-9d4b-267b408a49c9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
21275a38-5e09-44e5-9d4b-267b408a49c9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
21275a38-5e09-44e5-9d4b-267b408a49c9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
21275a38-5e09-44e5-9d4b-267b408a49c9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
21275a38-5e09-44e5-9d4b-267b408a49c9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
21275a38-5e09-44e5-9d4b-267b408a49c9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
21275a38-5e09-44e5-9d4b-267b408a49c9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
21275a38-5e09-44e5-9d4b-267b408a49c9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
5d24c01e-bd2a-4eda-a6fd-ed875e25ee63,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Table 1.1: Atrial fibrillation summary.,True,fibrillatory,,,,
bd8f1fe6-0a0a-4bbd-a1e1-fa9b13697f36,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Atrial Flutter,False,Atrial Flutter,,,,
da38463e-ac43-4e78-86b4-57526a3d771a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
da38463e-ac43-4e78-86b4-57526a3d771a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
da38463e-ac43-4e78-86b4-57526a3d771a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
da38463e-ac43-4e78-86b4-57526a3d771a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
da38463e-ac43-4e78-86b4-57526a3d771a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
da38463e-ac43-4e78-86b4-57526a3d771a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
da38463e-ac43-4e78-86b4-57526a3d771a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
da38463e-ac43-4e78-86b4-57526a3d771a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
da38463e-ac43-4e78-86b4-57526a3d771a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
da38463e-ac43-4e78-86b4-57526a3d771a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
da38463e-ac43-4e78-86b4-57526a3d771a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
da38463e-ac43-4e78-86b4-57526a3d771a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
da38463e-ac43-4e78-86b4-57526a3d771a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
da38463e-ac43-4e78-86b4-57526a3d771a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
da38463e-ac43-4e78-86b4-57526a3d771a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
da38463e-ac43-4e78-86b4-57526a3d771a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
da38463e-ac43-4e78-86b4-57526a3d771a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
412a2887-e8b1-4b33-b4e4-1c821f12c0c1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,macroreentrant,False,macroreentrant,,,,
e35db542-36de-4973-bb43-dc98a9deaf8a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,cavotricuspid,False,cavotricuspid,,,,
8f1f3a54-06df-4e2e-be77-6d700c86757d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"As with atrial fibrillation, the AV node’s refractory period prevents most of the P-waves from progressing to the ventricle, but commonly the AV conduction will be 2-to-1, so with an atrial rate of 300 bpm the ventricular rate will be 150 bpm. Parasympathetic stimulation or changes in AV node refractoriness can modify how many P-waves pass into the ventricle, but the the resultant rhythm is “regularly irregular.” When the heart rate is elevated, then distinguishing flutter from fibrillation becomes challenging and slowing ventricular rate pharmaceutically (adenosine) helps the flutter waves reemerge for a definitive diagnosis to be made.",True,cavotricuspid,,,,
cc043491-43cb-438b-aff5-59069f407a45,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Table 1.2: Atrial flutter summary.,True,cavotricuspid,,,,
109a2622-c929-473d-9990-f27b4667d83f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Multifocal Atrial Tachycardia,False,Multifocal Atrial Tachycardia,,,,
b6a69b0d-d67c-423b-ba19-972e6aa43476,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
b6a69b0d-d67c-423b-ba19-972e6aa43476,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
b6a69b0d-d67c-423b-ba19-972e6aa43476,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
b6a69b0d-d67c-423b-ba19-972e6aa43476,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
b6a69b0d-d67c-423b-ba19-972e6aa43476,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
b6a69b0d-d67c-423b-ba19-972e6aa43476,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
b6a69b0d-d67c-423b-ba19-972e6aa43476,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
b6a69b0d-d67c-423b-ba19-972e6aa43476,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
b6a69b0d-d67c-423b-ba19-972e6aa43476,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
b6a69b0d-d67c-423b-ba19-972e6aa43476,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
b6a69b0d-d67c-423b-ba19-972e6aa43476,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
b6a69b0d-d67c-423b-ba19-972e6aa43476,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
b6a69b0d-d67c-423b-ba19-972e6aa43476,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
b6a69b0d-d67c-423b-ba19-972e6aa43476,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
b6a69b0d-d67c-423b-ba19-972e6aa43476,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
b6a69b0d-d67c-423b-ba19-972e6aa43476,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
b6a69b0d-d67c-423b-ba19-972e6aa43476,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
e7a03e17-4f81-4202-be0d-174e38317cf3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"MAT frequently occurs in the setting of severe lung disease and, more specifically, during an exacerbation of lung disease. This rhythm is benign, and once the underlying lung disease is treated, it should resolve.",True,Multifocal Atrial Tachycardia,,,,
c0a190bf-1080-4130-8364-1b4114d3b9c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Table 1.3: MAT summary.,True,Multifocal Atrial Tachycardia,,,,
bc39049f-c57a-4676-ac21-f7a5f21d85d1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Premature Atrial Contraction,False,Premature Atrial Contraction,,,,
187f1d47-b653-4041-93c1-482312d2a7c8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A premature atrial contraction (PAC) is generated by a depolarization instigated outside of the SA node. This produces an extra P-wave, and consequently a shortening from previous P-P intervals is seen. The aberrant P-wave also has a different morphology from a sinus P-wave because of its different anatomical origin.",True,Premature Atrial Contraction,,,,
67f29fea-0988-4f66-9d15-62edf191a74f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
67f29fea-0988-4f66-9d15-62edf191a74f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
67f29fea-0988-4f66-9d15-62edf191a74f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
67f29fea-0988-4f66-9d15-62edf191a74f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
67f29fea-0988-4f66-9d15-62edf191a74f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
67f29fea-0988-4f66-9d15-62edf191a74f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
67f29fea-0988-4f66-9d15-62edf191a74f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
67f29fea-0988-4f66-9d15-62edf191a74f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
67f29fea-0988-4f66-9d15-62edf191a74f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
67f29fea-0988-4f66-9d15-62edf191a74f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
67f29fea-0988-4f66-9d15-62edf191a74f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
67f29fea-0988-4f66-9d15-62edf191a74f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
67f29fea-0988-4f66-9d15-62edf191a74f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
67f29fea-0988-4f66-9d15-62edf191a74f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
67f29fea-0988-4f66-9d15-62edf191a74f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
67f29fea-0988-4f66-9d15-62edf191a74f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
67f29fea-0988-4f66-9d15-62edf191a74f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
4e4f53c8-ed9f-4172-a4d1-aa03c8d2d056,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"If a PAC occurs when the AV node has not yet recovered from its refractory period, the PAC will fail to conduct to the ventricles; meaning the PAC will not be followed by a QRS complex or the ectopic P-R interval will be prolonged. The ECG will show a premature, ectopic P-wave and then no QRS complex afterward. When this occurs along with bigeminy, the ECG can appear as if there is sinus bradycardia.",True,Premature Atrial Contraction,,,,
7ecd770a-2f3a-4486-a514-c07bf259911b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Table 1.4: PAC summary.,True,Premature Atrial Contraction,,,,
be763113-62ca-445d-84a8-e42c3bc6de41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Sinus Bradycardia,False,Sinus Bradycardia,,,,
5ae4ac99-acfd-4398-bc7e-95220641f238,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Sinus bradycardia denotes a sinus rhythm below 60 bpm. Otherwise the ECG waveform is normal on an ECG with an upright P-wave in lead II preceding every QRS complex. There are many intrinsic causes associated with the heart itself, as well as extrinsic causes, some of which are listed table 1.5. Sinus bradycardia is usually asymptomatic as rates of 40–50 bpm can maintain hemodynamic stability. Rates below this can produce symptoms of fatigue, dizziness, and dyspnea on exertion.",True,Sinus Bradycardia,,,,
93245189-d042-4a77-8455-0d1c892e0204,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Table 1.5: Intrinsic and extrinsic causes associated with the heart.,True,Sinus Bradycardia,,,,
06697b49-9e22-4050-ad5d-4e3104c39b1c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Table 1.6: Sinus bradycardia summary.,True,Sinus Bradycardia,,,,
ba6a0897-e7a5-4438-95a0-fe3ac2113e70,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Premature Ventricular Contractions,False,Premature Ventricular Contractions,,,,
d463a6f0-935e-4325-bfae-0e7672fd213c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
d463a6f0-935e-4325-bfae-0e7672fd213c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
d463a6f0-935e-4325-bfae-0e7672fd213c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
d463a6f0-935e-4325-bfae-0e7672fd213c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
d463a6f0-935e-4325-bfae-0e7672fd213c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
d463a6f0-935e-4325-bfae-0e7672fd213c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
d463a6f0-935e-4325-bfae-0e7672fd213c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
d463a6f0-935e-4325-bfae-0e7672fd213c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
d463a6f0-935e-4325-bfae-0e7672fd213c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
d463a6f0-935e-4325-bfae-0e7672fd213c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
d463a6f0-935e-4325-bfae-0e7672fd213c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
d463a6f0-935e-4325-bfae-0e7672fd213c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
d463a6f0-935e-4325-bfae-0e7672fd213c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
d463a6f0-935e-4325-bfae-0e7672fd213c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
d463a6f0-935e-4325-bfae-0e7672fd213c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
d463a6f0-935e-4325-bfae-0e7672fd213c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
d463a6f0-935e-4325-bfae-0e7672fd213c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
bd7a53c4-1537-46f6-a836-cd20512a5290,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Table 1.7: PVC summary.,True,Premature Ventricular Contractions,,,,
eeccce5b-c72b-471d-a49a-dac60b778aaa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Ventricular Tachycardia,False,Ventricular Tachycardia,,,,
9682b6a6-0bcc-4658-b7c2-a904a27bb8b7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Ventricular tachycardia (VT) is caused by reentry currents being established in the ventricular myocardium or groups of ventricular myocytes that have aberrant electrical behavior. As such, VT is usually caused by underlying cardiac disease.",True,Ventricular Tachycardia,,,,
0f82e535-8871-416a-89cf-5fff571ab94c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Like a PVC, the aberrant depolarizations do not follow the normal conduction pathways so are wide (>120 msecs), but unlike a PVC, VT involves a ventricular rate >100 bpm. With disorganized contractility and reduced filling time, VT can lead to hemodynamic instability and severe hypotension—hence it is life threatening.",True,Ventricular Tachycardia,,,,
1bbd8c7a-4f09-4699-aace-9f6f21d228a5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The QRS morphology in VT is highly variable between patients and depends on where the arrhythmia originates. Consequently there are several ways to classify VT based on duration, symptoms, QRS morphology, rate, and origin.",True,Ventricular Tachycardia,,,,
2b1225bb-a46c-4cbf-a775-17ebfd155672,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Sustained VT is any VT that lasts for more than 30 seconds or is symptomatic. Nonsustained VT lasts for less than 30 seconds and is asymptomatic.,True,Ventricular Tachycardia,,,,
b369cf51-54a4-4249-a00e-69fb64d4690f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b369cf51-54a4-4249-a00e-69fb64d4690f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b369cf51-54a4-4249-a00e-69fb64d4690f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b369cf51-54a4-4249-a00e-69fb64d4690f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b369cf51-54a4-4249-a00e-69fb64d4690f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b369cf51-54a4-4249-a00e-69fb64d4690f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b369cf51-54a4-4249-a00e-69fb64d4690f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b369cf51-54a4-4249-a00e-69fb64d4690f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b369cf51-54a4-4249-a00e-69fb64d4690f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b369cf51-54a4-4249-a00e-69fb64d4690f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b369cf51-54a4-4249-a00e-69fb64d4690f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b369cf51-54a4-4249-a00e-69fb64d4690f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b369cf51-54a4-4249-a00e-69fb64d4690f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b369cf51-54a4-4249-a00e-69fb64d4690f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b369cf51-54a4-4249-a00e-69fb64d4690f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b369cf51-54a4-4249-a00e-69fb64d4690f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b369cf51-54a4-4249-a00e-69fb64d4690f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
666f2ed8-0d8a-43dc-9c68-3139236d2aeb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
666f2ed8-0d8a-43dc-9c68-3139236d2aeb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
666f2ed8-0d8a-43dc-9c68-3139236d2aeb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
666f2ed8-0d8a-43dc-9c68-3139236d2aeb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
666f2ed8-0d8a-43dc-9c68-3139236d2aeb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
666f2ed8-0d8a-43dc-9c68-3139236d2aeb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
666f2ed8-0d8a-43dc-9c68-3139236d2aeb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
666f2ed8-0d8a-43dc-9c68-3139236d2aeb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
666f2ed8-0d8a-43dc-9c68-3139236d2aeb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
666f2ed8-0d8a-43dc-9c68-3139236d2aeb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
666f2ed8-0d8a-43dc-9c68-3139236d2aeb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
666f2ed8-0d8a-43dc-9c68-3139236d2aeb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
666f2ed8-0d8a-43dc-9c68-3139236d2aeb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
666f2ed8-0d8a-43dc-9c68-3139236d2aeb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
666f2ed8-0d8a-43dc-9c68-3139236d2aeb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
666f2ed8-0d8a-43dc-9c68-3139236d2aeb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
666f2ed8-0d8a-43dc-9c68-3139236d2aeb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
34d9ae24-6017-48c2-9fdd-20b10f68b065,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Torsades de pointes is associated with a prolonged QT interval (>600 msecs) that helps distinguish it from other forms of polymorphous VT. The longer QT interval can be caused by ionic abnormalities that reduce the repolarizing current of Phase 3 of the cardiac action potential. This makes the myocardium susceptible to early after-depolarizations—the trigger for torsades de pointes. These after-depolarizations do not happen uniformly across the myocardium and are more common in endocardial tissue where the repolarization currents are slower. So torsades de pointes arises from the after-depolarizations causing reentry currents in neighboring tissue.,True,Ventricular Tachycardia,,,,
29aa56cd-3268-4fe9-9ad2-a2485284cdcb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Both common garden variety VTs and torsades de pointes can progress to ventricular fibrillation.,True,Ventricular Tachycardia,,,,
496b8ad0-12e0-4b0b-831b-aeb6f85a3032,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Table 1.8: VT summary.,True,Ventricular Tachycardia,,,,
cf1ad433-5ee7-4830-b4af-eaacdce6892c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Ventricular Fibrillation,False,Ventricular Fibrillation,,,,
29f1c7e0-66db-4193-b154-03ac390bb17a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Ventricular fibrillation (VF) occurs when the ventricular rate exceeds 400 bpm. The disorganized and uncoordinated contraction of the myocardium causes cardiac output to fall to catastrophic levels. Rates of survival for out-of-hospital VF are low.,True,Ventricular Fibrillation,,,,
85c60c1d-ace5-489a-94db-9f1f5f562d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
85c60c1d-ace5-489a-94db-9f1f5f562d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
85c60c1d-ace5-489a-94db-9f1f5f562d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
85c60c1d-ace5-489a-94db-9f1f5f562d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
85c60c1d-ace5-489a-94db-9f1f5f562d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
85c60c1d-ace5-489a-94db-9f1f5f562d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
85c60c1d-ace5-489a-94db-9f1f5f562d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
85c60c1d-ace5-489a-94db-9f1f5f562d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
85c60c1d-ace5-489a-94db-9f1f5f562d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
85c60c1d-ace5-489a-94db-9f1f5f562d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
85c60c1d-ace5-489a-94db-9f1f5f562d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
85c60c1d-ace5-489a-94db-9f1f5f562d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
85c60c1d-ace5-489a-94db-9f1f5f562d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
85c60c1d-ace5-489a-94db-9f1f5f562d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
85c60c1d-ace5-489a-94db-9f1f5f562d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
85c60c1d-ace5-489a-94db-9f1f5f562d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
85c60c1d-ace5-489a-94db-9f1f5f562d20,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
95b189c1-5b39-4049-9d2d-a4e7596edb3d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Table 1.9: VF summary.,True,Ventricular Fibrillation,,,,
dd160b74-0c9d-4805-8f65-e688cbb9508f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,First-Degree Atrioventricular Block,False,First-Degree Atrioventricular Block,,,,
6bfe7ed9-9a0b-4d0b-9fdb-71326ff2fcd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6bfe7ed9-9a0b-4d0b-9fdb-71326ff2fcd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6bfe7ed9-9a0b-4d0b-9fdb-71326ff2fcd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6bfe7ed9-9a0b-4d0b-9fdb-71326ff2fcd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6bfe7ed9-9a0b-4d0b-9fdb-71326ff2fcd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6bfe7ed9-9a0b-4d0b-9fdb-71326ff2fcd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6bfe7ed9-9a0b-4d0b-9fdb-71326ff2fcd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6bfe7ed9-9a0b-4d0b-9fdb-71326ff2fcd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6bfe7ed9-9a0b-4d0b-9fdb-71326ff2fcd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6bfe7ed9-9a0b-4d0b-9fdb-71326ff2fcd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6bfe7ed9-9a0b-4d0b-9fdb-71326ff2fcd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6bfe7ed9-9a0b-4d0b-9fdb-71326ff2fcd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6bfe7ed9-9a0b-4d0b-9fdb-71326ff2fcd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6bfe7ed9-9a0b-4d0b-9fdb-71326ff2fcd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6bfe7ed9-9a0b-4d0b-9fdb-71326ff2fcd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6bfe7ed9-9a0b-4d0b-9fdb-71326ff2fcd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
6bfe7ed9-9a0b-4d0b-9fdb-71326ff2fcd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
23f4316d-53cb-4b68-95ea-cf77a7ca9acb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
23f4316d-53cb-4b68-95ea-cf77a7ca9acb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
23f4316d-53cb-4b68-95ea-cf77a7ca9acb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
23f4316d-53cb-4b68-95ea-cf77a7ca9acb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
23f4316d-53cb-4b68-95ea-cf77a7ca9acb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
23f4316d-53cb-4b68-95ea-cf77a7ca9acb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
23f4316d-53cb-4b68-95ea-cf77a7ca9acb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
23f4316d-53cb-4b68-95ea-cf77a7ca9acb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
23f4316d-53cb-4b68-95ea-cf77a7ca9acb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
23f4316d-53cb-4b68-95ea-cf77a7ca9acb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
23f4316d-53cb-4b68-95ea-cf77a7ca9acb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
23f4316d-53cb-4b68-95ea-cf77a7ca9acb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
23f4316d-53cb-4b68-95ea-cf77a7ca9acb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
23f4316d-53cb-4b68-95ea-cf77a7ca9acb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
23f4316d-53cb-4b68-95ea-cf77a7ca9acb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
23f4316d-53cb-4b68-95ea-cf77a7ca9acb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
23f4316d-53cb-4b68-95ea-cf77a7ca9acb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
aba3cac3-021c-4fb0-9005-43bb40db8bcf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Table 1.10: First-degree block summary.,True,First-Degree Atrioventricular Block,,,,
864e7ce0-c4fe-4269-85be-091b81d0c7cc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Second-Degree Atrioventricular Block,False,Second-Degree Atrioventricular Block,,,,
006e5348-1836-4749-aaeb-213abe2a49d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A second-degree atrioventricular block also has changes in P-R interval, but it starts to show failure of the P-wave to propagate a QRS complex every time (i.e., intermittently the depolarization fails to reach the ventricles). The pattern of missed ventricular depolarizations, or blocked P-waves, is often very regular and described as a ratio of P-waves to QRS complex. The way in which the P-R interval changes in relation to the blocked P-waves produces subclassifications of second-degree blocks, Mobitz I and II.",True,Second-Degree Atrioventricular Block,,,,
9b4ef857-4762-41d1-9410-5e2144b7c770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9b4ef857-4762-41d1-9410-5e2144b7c770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9b4ef857-4762-41d1-9410-5e2144b7c770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9b4ef857-4762-41d1-9410-5e2144b7c770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9b4ef857-4762-41d1-9410-5e2144b7c770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9b4ef857-4762-41d1-9410-5e2144b7c770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9b4ef857-4762-41d1-9410-5e2144b7c770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9b4ef857-4762-41d1-9410-5e2144b7c770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9b4ef857-4762-41d1-9410-5e2144b7c770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9b4ef857-4762-41d1-9410-5e2144b7c770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9b4ef857-4762-41d1-9410-5e2144b7c770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9b4ef857-4762-41d1-9410-5e2144b7c770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9b4ef857-4762-41d1-9410-5e2144b7c770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9b4ef857-4762-41d1-9410-5e2144b7c770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9b4ef857-4762-41d1-9410-5e2144b7c770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9b4ef857-4762-41d1-9410-5e2144b7c770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
9b4ef857-4762-41d1-9410-5e2144b7c770,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
811ee2e4-4aeb-496b-a55d-1320bc013d49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
811ee2e4-4aeb-496b-a55d-1320bc013d49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
811ee2e4-4aeb-496b-a55d-1320bc013d49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
811ee2e4-4aeb-496b-a55d-1320bc013d49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
811ee2e4-4aeb-496b-a55d-1320bc013d49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
811ee2e4-4aeb-496b-a55d-1320bc013d49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
811ee2e4-4aeb-496b-a55d-1320bc013d49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
811ee2e4-4aeb-496b-a55d-1320bc013d49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
811ee2e4-4aeb-496b-a55d-1320bc013d49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
811ee2e4-4aeb-496b-a55d-1320bc013d49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
811ee2e4-4aeb-496b-a55d-1320bc013d49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
811ee2e4-4aeb-496b-a55d-1320bc013d49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
811ee2e4-4aeb-496b-a55d-1320bc013d49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
811ee2e4-4aeb-496b-a55d-1320bc013d49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
811ee2e4-4aeb-496b-a55d-1320bc013d49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
811ee2e4-4aeb-496b-a55d-1320bc013d49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
811ee2e4-4aeb-496b-a55d-1320bc013d49,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
7c37300b-190f-4dc6-886f-d7dbeba3e68d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Table 1.11: Second-degree block summary.,True,Second-Degree Atrioventricular Block,,,,
0280bb89-7f1e-40ad-91c5-5999d4cc45af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Third-Degree Atrioventricular Block,False,Third-Degree Atrioventricular Block,,,,
7dec5618-f1d7-426e-9391-77e3a19e416d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
7dec5618-f1d7-426e-9391-77e3a19e416d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
7dec5618-f1d7-426e-9391-77e3a19e416d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
7dec5618-f1d7-426e-9391-77e3a19e416d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
7dec5618-f1d7-426e-9391-77e3a19e416d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
7dec5618-f1d7-426e-9391-77e3a19e416d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
7dec5618-f1d7-426e-9391-77e3a19e416d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
7dec5618-f1d7-426e-9391-77e3a19e416d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
7dec5618-f1d7-426e-9391-77e3a19e416d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
7dec5618-f1d7-426e-9391-77e3a19e416d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
7dec5618-f1d7-426e-9391-77e3a19e416d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
7dec5618-f1d7-426e-9391-77e3a19e416d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
7dec5618-f1d7-426e-9391-77e3a19e416d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
7dec5618-f1d7-426e-9391-77e3a19e416d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
7dec5618-f1d7-426e-9391-77e3a19e416d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
7dec5618-f1d7-426e-9391-77e3a19e416d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
7dec5618-f1d7-426e-9391-77e3a19e416d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
696074da-86cb-48b0-a768-1c626a902d6e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Table 1.12: Third-degree block summary.,True,Third-Degree Atrioventricular Block,,,,
9e39c243-e075-4033-96d6-6d033b888fb4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Left Bundle Branch Block,False,Left Bundle Branch Block,,,,
26ada8d7-ab1f-491d-b1f0-70d3a1b3945f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"A left bundle branch block (LBBB) is generated when the conductivity of the His-Purkinje system in the left ventricle is compromised, either through damage or disease. The ECG changes, and criteria for LBBB relate to these changes in conductivity and the left-side location.",True,Left Bundle Branch Block,,,,
c720e2f2-1829-494c-9946-c26ff52ad482,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c720e2f2-1829-494c-9946-c26ff52ad482,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c720e2f2-1829-494c-9946-c26ff52ad482,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c720e2f2-1829-494c-9946-c26ff52ad482,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c720e2f2-1829-494c-9946-c26ff52ad482,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c720e2f2-1829-494c-9946-c26ff52ad482,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c720e2f2-1829-494c-9946-c26ff52ad482,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c720e2f2-1829-494c-9946-c26ff52ad482,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c720e2f2-1829-494c-9946-c26ff52ad482,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c720e2f2-1829-494c-9946-c26ff52ad482,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c720e2f2-1829-494c-9946-c26ff52ad482,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c720e2f2-1829-494c-9946-c26ff52ad482,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c720e2f2-1829-494c-9946-c26ff52ad482,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c720e2f2-1829-494c-9946-c26ff52ad482,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c720e2f2-1829-494c-9946-c26ff52ad482,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c720e2f2-1829-494c-9946-c26ff52ad482,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
c720e2f2-1829-494c-9946-c26ff52ad482,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
474f29a1-ee06-4727-9e19-7e1da0dfbd28,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The lateral leads (I, V5, and V6) normally show a downward deflecting Q-wave as normal septal deflection initially occurs left-to-right (i.e., away from the lateral leads). In LBBB the change in direction to right-to-left, plus the longer duration, eliminates the Q-wave from the lateral leads, and Q-waves will be small in aVL.",True,Left Bundle Branch Block,,,,
c1b88c35-979e-4a54-b002-cdd58067c80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
c1b88c35-979e-4a54-b002-cdd58067c80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
c1b88c35-979e-4a54-b002-cdd58067c80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
c1b88c35-979e-4a54-b002-cdd58067c80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
c1b88c35-979e-4a54-b002-cdd58067c80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
c1b88c35-979e-4a54-b002-cdd58067c80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
c1b88c35-979e-4a54-b002-cdd58067c80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
c1b88c35-979e-4a54-b002-cdd58067c80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
c1b88c35-979e-4a54-b002-cdd58067c80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
c1b88c35-979e-4a54-b002-cdd58067c80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
c1b88c35-979e-4a54-b002-cdd58067c80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
c1b88c35-979e-4a54-b002-cdd58067c80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
c1b88c35-979e-4a54-b002-cdd58067c80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
c1b88c35-979e-4a54-b002-cdd58067c80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
c1b88c35-979e-4a54-b002-cdd58067c80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
c1b88c35-979e-4a54-b002-cdd58067c80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
c1b88c35-979e-4a54-b002-cdd58067c80f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
01204dd6-aee8-4432-b2dd-ce0842bdb099,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
01204dd6-aee8-4432-b2dd-ce0842bdb099,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
01204dd6-aee8-4432-b2dd-ce0842bdb099,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
01204dd6-aee8-4432-b2dd-ce0842bdb099,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
01204dd6-aee8-4432-b2dd-ce0842bdb099,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
01204dd6-aee8-4432-b2dd-ce0842bdb099,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
01204dd6-aee8-4432-b2dd-ce0842bdb099,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
01204dd6-aee8-4432-b2dd-ce0842bdb099,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
01204dd6-aee8-4432-b2dd-ce0842bdb099,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
01204dd6-aee8-4432-b2dd-ce0842bdb099,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
01204dd6-aee8-4432-b2dd-ce0842bdb099,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
01204dd6-aee8-4432-b2dd-ce0842bdb099,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
01204dd6-aee8-4432-b2dd-ce0842bdb099,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
01204dd6-aee8-4432-b2dd-ce0842bdb099,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
01204dd6-aee8-4432-b2dd-ce0842bdb099,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
01204dd6-aee8-4432-b2dd-ce0842bdb099,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
01204dd6-aee8-4432-b2dd-ce0842bdb099,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
8383319a-1c01-4ab6-828c-78e5eb29bc9b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Table 1.13: LBBB summary.,True,Left Bundle Branch Block,,,,
fa029fab-6832-4774-96fd-b5c60010b0b3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Right Bundle Branch Block,False,Right Bundle Branch Block,,,,
e73973dd-3548-40a3-9f19-53a51cb1c37b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The causes and manifestations of a right bundle branch block (RBBB) bear some similarities to those described for LBBB, but of course this time its depolarization of the right ventricle is delayed. Causes of RBBB include ischemic heart disease again as well as other myocardial diseases, but pulmonary issues such as pulmonary embolism and cor pulmonale can be added to the list.",True,Right Bundle Branch Block,,,,
153d8367-5787-4670-bf24-e060a0a0dc09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
153d8367-5787-4670-bf24-e060a0a0dc09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
153d8367-5787-4670-bf24-e060a0a0dc09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
153d8367-5787-4670-bf24-e060a0a0dc09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
153d8367-5787-4670-bf24-e060a0a0dc09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
153d8367-5787-4670-bf24-e060a0a0dc09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
153d8367-5787-4670-bf24-e060a0a0dc09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
153d8367-5787-4670-bf24-e060a0a0dc09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
153d8367-5787-4670-bf24-e060a0a0dc09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
153d8367-5787-4670-bf24-e060a0a0dc09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
153d8367-5787-4670-bf24-e060a0a0dc09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
153d8367-5787-4670-bf24-e060a0a0dc09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
153d8367-5787-4670-bf24-e060a0a0dc09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
153d8367-5787-4670-bf24-e060a0a0dc09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
153d8367-5787-4670-bf24-e060a0a0dc09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
153d8367-5787-4670-bf24-e060a0a0dc09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
153d8367-5787-4670-bf24-e060a0a0dc09,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
102b5b18-ec5a-4ecf-9107-0e73e8e4c315,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Table 1.14: RBBB summary.,True,Right Bundle Branch Block,,,,
ee99e894-4d8d-42e4-a88b-1b996e9b0f3b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Wolff-Parkinson-White Syndrome,False,Wolff-Parkinson-White Syndrome,,,,
c591d42a-bb63-43d7-b1d9-eb2868d78655,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Normally the only electrical connection between the atria and the ventricles is the AV node. Otherwise the fibrous skeleton of the heart electrically insulates the atria from the ventricles. In Wolff-Parkinson-White (WPW) syndrome, that insulation is incomplete, and an “accessory pathway” connects the electrical system of the atria directly to the ventricles. If you think of the AV node as a bridge over the fibrous wall with regulated access, the accessory pathway is like a pathological tunnel under it with no regulation.",True,Wolff-Parkinson-White Syndrome,,,,
70b649e0-81cb-4c0e-a3a6-5ced17a36296,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
70b649e0-81cb-4c0e-a3a6-5ced17a36296,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
70b649e0-81cb-4c0e-a3a6-5ced17a36296,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
70b649e0-81cb-4c0e-a3a6-5ced17a36296,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
70b649e0-81cb-4c0e-a3a6-5ced17a36296,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
70b649e0-81cb-4c0e-a3a6-5ced17a36296,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
70b649e0-81cb-4c0e-a3a6-5ced17a36296,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
70b649e0-81cb-4c0e-a3a6-5ced17a36296,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
70b649e0-81cb-4c0e-a3a6-5ced17a36296,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
70b649e0-81cb-4c0e-a3a6-5ced17a36296,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
70b649e0-81cb-4c0e-a3a6-5ced17a36296,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
70b649e0-81cb-4c0e-a3a6-5ced17a36296,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
70b649e0-81cb-4c0e-a3a6-5ced17a36296,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
70b649e0-81cb-4c0e-a3a6-5ced17a36296,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
70b649e0-81cb-4c0e-a3a6-5ced17a36296,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
70b649e0-81cb-4c0e-a3a6-5ced17a36296,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
70b649e0-81cb-4c0e-a3a6-5ced17a36296,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
71437fdf-6b81-4fd3-ba8b-13e5e52c0751,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"WPW syndrome is often asymptomatic, and patients do not require immediate treatment. However, if atrial fibrillation occurs in a WPW patient, the accessory pathway can allow the atrial fibrillation waves through to the ventricle (with no AV nodal refractory period to prevent them). Consequently a high ventricular rate is seen, and the risk of ventricular fibrillation being established means immediate clinical attention is required.",True,Wolff-Parkinson-White Syndrome,,,,
dc4e10a1-512d-460b-9b6d-cc3d5a0f21db,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Hyper- and Hypocalcemia,False,Hyper- and Hypocalcemia,,,,
0824253b-1724-489d-b006-53eb62a174f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
0824253b-1724-489d-b006-53eb62a174f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
0824253b-1724-489d-b006-53eb62a174f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
0824253b-1724-489d-b006-53eb62a174f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
0824253b-1724-489d-b006-53eb62a174f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
0824253b-1724-489d-b006-53eb62a174f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
0824253b-1724-489d-b006-53eb62a174f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
0824253b-1724-489d-b006-53eb62a174f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
0824253b-1724-489d-b006-53eb62a174f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
0824253b-1724-489d-b006-53eb62a174f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
0824253b-1724-489d-b006-53eb62a174f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
0824253b-1724-489d-b006-53eb62a174f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
0824253b-1724-489d-b006-53eb62a174f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
0824253b-1724-489d-b006-53eb62a174f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
0824253b-1724-489d-b006-53eb62a174f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
0824253b-1724-489d-b006-53eb62a174f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
0824253b-1724-489d-b006-53eb62a174f7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
6d5406b3-3622-4f9d-9442-76e1f550e2b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
6d5406b3-3622-4f9d-9442-76e1f550e2b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
6d5406b3-3622-4f9d-9442-76e1f550e2b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
6d5406b3-3622-4f9d-9442-76e1f550e2b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
6d5406b3-3622-4f9d-9442-76e1f550e2b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
6d5406b3-3622-4f9d-9442-76e1f550e2b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
6d5406b3-3622-4f9d-9442-76e1f550e2b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
6d5406b3-3622-4f9d-9442-76e1f550e2b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
6d5406b3-3622-4f9d-9442-76e1f550e2b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
6d5406b3-3622-4f9d-9442-76e1f550e2b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
6d5406b3-3622-4f9d-9442-76e1f550e2b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
6d5406b3-3622-4f9d-9442-76e1f550e2b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
6d5406b3-3622-4f9d-9442-76e1f550e2b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
6d5406b3-3622-4f9d-9442-76e1f550e2b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
6d5406b3-3622-4f9d-9442-76e1f550e2b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
6d5406b3-3622-4f9d-9442-76e1f550e2b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
6d5406b3-3622-4f9d-9442-76e1f550e2b2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
95075dc6-93a5-404b-9062-074ffe1bbbb1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Table 1.16: Hyper- and hypocalcemia summary.,True,Hyper- and Hypocalcemia,,,,
62f66502-1647-4000-a2e7-3175e9cc6e9b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Hyper- and Hypokalemia,False,Hyper- and Hypokalemia,,,,
9b2cd328-fd23-405a-9268-5b3fb40ac6b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"The pathophysiology is not as simple as changes in extracellular K+ changing the electrochemical gradient for K+. Because of potassium’s role in maintaining the resting membrane potential, shifts in extracellular potassium can also influence the activity of Na+ and Ca++ channels.",True,Hyper- and Hypokalemia,,,,
ce1373c6-69e1-4ddd-a76c-ba8b78dde46f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ce1373c6-69e1-4ddd-a76c-ba8b78dde46f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ce1373c6-69e1-4ddd-a76c-ba8b78dde46f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ce1373c6-69e1-4ddd-a76c-ba8b78dde46f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ce1373c6-69e1-4ddd-a76c-ba8b78dde46f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ce1373c6-69e1-4ddd-a76c-ba8b78dde46f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ce1373c6-69e1-4ddd-a76c-ba8b78dde46f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ce1373c6-69e1-4ddd-a76c-ba8b78dde46f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ce1373c6-69e1-4ddd-a76c-ba8b78dde46f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ce1373c6-69e1-4ddd-a76c-ba8b78dde46f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ce1373c6-69e1-4ddd-a76c-ba8b78dde46f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ce1373c6-69e1-4ddd-a76c-ba8b78dde46f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ce1373c6-69e1-4ddd-a76c-ba8b78dde46f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ce1373c6-69e1-4ddd-a76c-ba8b78dde46f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ce1373c6-69e1-4ddd-a76c-ba8b78dde46f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ce1373c6-69e1-4ddd-a76c-ba8b78dde46f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
ce1373c6-69e1-4ddd-a76c-ba8b78dde46f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
cd68b597-90ea-4c80-8a9a-befca41a6298,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"As hypokalemia also inhibits Na+-K+ ATPase, Na+ accumulates inside the cell. This in turn leads to an accumulation of Ca++ because of a subsequent failure of the Na+-Ca++ exchanger. Extended presence of these two positive ions inside the myocyte prolongs the action potential and may manifest as an increased width and amplitude of the P-wave.",True,Hyper- and Hypokalemia,,,,
cf318d90-9dd6-45f7-873f-57aedce25870,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"As hypokalemia worsens, the problems with K+ conductance and repolarization increase, and the myocardium becomes susceptible to early after-depolarization (EAD) arrhythmias.",True,Hyper- and Hypokalemia,,,,
170dd510-92ef-4c38-934a-435215fa6d6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
170dd510-92ef-4c38-934a-435215fa6d6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
170dd510-92ef-4c38-934a-435215fa6d6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
170dd510-92ef-4c38-934a-435215fa6d6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
170dd510-92ef-4c38-934a-435215fa6d6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
170dd510-92ef-4c38-934a-435215fa6d6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
170dd510-92ef-4c38-934a-435215fa6d6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
170dd510-92ef-4c38-934a-435215fa6d6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
170dd510-92ef-4c38-934a-435215fa6d6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
170dd510-92ef-4c38-934a-435215fa6d6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
170dd510-92ef-4c38-934a-435215fa6d6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
170dd510-92ef-4c38-934a-435215fa6d6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
170dd510-92ef-4c38-934a-435215fa6d6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
170dd510-92ef-4c38-934a-435215fa6d6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
170dd510-92ef-4c38-934a-435215fa6d6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
170dd510-92ef-4c38-934a-435215fa6d6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
170dd510-92ef-4c38-934a-435215fa6d6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
b4ec0e07-85ef-4e0b-8af7-662a6140cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
b4ec0e07-85ef-4e0b-8af7-662a6140cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
b4ec0e07-85ef-4e0b-8af7-662a6140cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
b4ec0e07-85ef-4e0b-8af7-662a6140cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
b4ec0e07-85ef-4e0b-8af7-662a6140cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
b4ec0e07-85ef-4e0b-8af7-662a6140cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
b4ec0e07-85ef-4e0b-8af7-662a6140cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
b4ec0e07-85ef-4e0b-8af7-662a6140cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
b4ec0e07-85ef-4e0b-8af7-662a6140cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
b4ec0e07-85ef-4e0b-8af7-662a6140cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
b4ec0e07-85ef-4e0b-8af7-662a6140cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
b4ec0e07-85ef-4e0b-8af7-662a6140cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
b4ec0e07-85ef-4e0b-8af7-662a6140cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
b4ec0e07-85ef-4e0b-8af7-662a6140cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
b4ec0e07-85ef-4e0b-8af7-662a6140cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
b4ec0e07-85ef-4e0b-8af7-662a6140cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
b4ec0e07-85ef-4e0b-8af7-662a6140cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
e1a8ec43-628e-48b8-922f-5d5c24b94f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e1a8ec43-628e-48b8-922f-5d5c24b94f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e1a8ec43-628e-48b8-922f-5d5c24b94f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e1a8ec43-628e-48b8-922f-5d5c24b94f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e1a8ec43-628e-48b8-922f-5d5c24b94f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e1a8ec43-628e-48b8-922f-5d5c24b94f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e1a8ec43-628e-48b8-922f-5d5c24b94f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e1a8ec43-628e-48b8-922f-5d5c24b94f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e1a8ec43-628e-48b8-922f-5d5c24b94f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e1a8ec43-628e-48b8-922f-5d5c24b94f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e1a8ec43-628e-48b8-922f-5d5c24b94f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e1a8ec43-628e-48b8-922f-5d5c24b94f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e1a8ec43-628e-48b8-922f-5d5c24b94f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e1a8ec43-628e-48b8-922f-5d5c24b94f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e1a8ec43-628e-48b8-922f-5d5c24b94f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e1a8ec43-628e-48b8-922f-5d5c24b94f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e1a8ec43-628e-48b8-922f-5d5c24b94f60,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
c231fb2d-e6d5-4f67-bd8e-d9ec26573ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
c231fb2d-e6d5-4f67-bd8e-d9ec26573ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
c231fb2d-e6d5-4f67-bd8e-d9ec26573ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
c231fb2d-e6d5-4f67-bd8e-d9ec26573ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
c231fb2d-e6d5-4f67-bd8e-d9ec26573ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
c231fb2d-e6d5-4f67-bd8e-d9ec26573ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
c231fb2d-e6d5-4f67-bd8e-d9ec26573ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
c231fb2d-e6d5-4f67-bd8e-d9ec26573ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
c231fb2d-e6d5-4f67-bd8e-d9ec26573ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
c231fb2d-e6d5-4f67-bd8e-d9ec26573ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
c231fb2d-e6d5-4f67-bd8e-d9ec26573ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
c231fb2d-e6d5-4f67-bd8e-d9ec26573ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
c231fb2d-e6d5-4f67-bd8e-d9ec26573ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
c231fb2d-e6d5-4f67-bd8e-d9ec26573ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
c231fb2d-e6d5-4f67-bd8e-d9ec26573ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
c231fb2d-e6d5-4f67-bd8e-d9ec26573ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
c231fb2d-e6d5-4f67-bd8e-d9ec26573ab1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
c9c34fbb-8c2a-4f31-af77-a08dfe3b000a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Table 1.17: Hypo- and hyperkalemia summary.,True,Hyper- and Hypokalemia,,,,
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b3d3daba-97f3-4842-929b-100a8a841338,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,Text,False,Text,,,,
ce638d0d-1616-4dab-be0d-3888b78eb990,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Burns, Ed, and Robert Buttner. Hypercalcaemia. Lift in the Fast Lane, 2021. https://litfl.com/hypercalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
0a25de3f-fa15-43ba-93d5-0c53b8a8f2e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Burns, Ed, and Robert Buttner. Hypocalcaemia. Life in the Fast Lane, 2021. https://litfl.com/hypocalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
da4d3013-5356-4655-a171-227aeb034367,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Buttner, Robert, and Ed Burns. Hyperkalaemia. Life in the Fast Lane. https://litfl.com/hyperkalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
0a5afea1-544a-43aa-a0fa-65e885f62139,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Buttner, Robert, and Ed Burns. Hypokalaemia. Life in the Fast Lane, 2021. https://litfl.com/hypokalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
ab03beda-7d84-45fa-9a81-2affea7d682c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Chhabra, Lovely, Amandeep Goyal, and Michael D. Benham. Wolff Parkinson White Syndrome. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK554437/, CC BY 4.0.",True,Text,,,,
0cd57bc3-6c74-45ec-a890-7ce45c90ef93,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Custer, Adam M., Varun S. Yelamanchili, and Sarah L. Lappin. Multifocal Atrial Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459152/, CC BY 4.0.",True,Text,,,,
02d2cde2-72cd-4b67-b420-e7851ee20804,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Farzam, Khashayar, and John R. Richards. Premature Ventricular Contraction. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532991/, CC BY 4.0.",True,Text,,,,
3658b043-032a-42f0-b672-631a8ee239ed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Foth, Christopher, Manesh Kumar Gangwani, and Heidi Alvey. Ventricular Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532954/, CC BY 4.0.",True,Text,,,,
1987fa9b-5636-47c1-876a-8f50791bacdf,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Hafeez, Yamama, and Shamai A. Grossman. Sinus Bradycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK493201/, CC BY 4.0.",True,Text,,,,
ca725cc8-2d2a-4431-85c9-635c0c2870fb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Harkness, Weston T., and Mary Hicks. Right Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK507872/, CC BY 4.0.",True,Text,,,,
a4b2bcc0-c5b1-42c4-9652-08e253c798e5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Heaton, Joseph, and Srikanth Yandrapalli. Premature Atrial Contractions. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK559204/, CC BY 4.0.",True,Text,,,,
72acf290-8e0d-4172-aa93-1157bc41988a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Kashou, Anthony H., Amandeep Goyal, Tran Nguyen, and Lovely Chhabra. Atrioventricular Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459147/, CC BY 4.0.",True,Text,,,,
2b488bcd-fc13-44d2-af25-29264584ac62,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,“Learn the Heart.” Healio. https://www.healio.com/cardiology/learn-the-heart.,True,Text,,,,
b357ecca-d930-436b-a1b3-837d0e0e6ebc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Ludhwani, Dipesh, Amandeep Goyal, and Mandar Jagtap. Ventricular Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK537120/, CC BY 4.0.",True,Text,,,,
2841b754-c325-4809-88f1-00801f6701ed,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Nesheiwat, Zeid, Amandeep Goyal, and Mandar Jagtap. Atrial Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK526072/, CC BY 4.0.",True,Text,,,,
5ec255fb-8545-4c99-9ddf-73d6ca70bc14,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Pipilas, Daniel C., Bruce A. Koplan, and Leonard S. Lilly. “The Electrocardiogram.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 4. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.",True,Text,,,,
75fdf802-7642-41f2-b038-00008c24cd33,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Rodriguez Ziccardi, Mary, Amandeep Goyal, and Christopher V. Maani. Atrial Flutter. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK540985/, CC BY 4.0.",True,Text,,,,
977fe084-eb38-4985-8864-03d983f661ab,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,Atrial Fibrillation,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/#chapter-25-section-1,"Scherbak, Dmitriy, and Gregory J. Hicks. Left Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK482167/, CC BY 4.0.",True,Text,,,,
750b16ee-1293-43c0-9e2f-7da640218bdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,USMLE,False,USMLE,,,,
4e3b2355-3a7a-40e8-81f8-feaa62fe36ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
4e3b2355-3a7a-40e8-81f8-feaa62fe36ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
4e3b2355-3a7a-40e8-81f8-feaa62fe36ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
4e3b2355-3a7a-40e8-81f8-feaa62fe36ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
4e3b2355-3a7a-40e8-81f8-feaa62fe36ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
4e3b2355-3a7a-40e8-81f8-feaa62fe36ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
4e3b2355-3a7a-40e8-81f8-feaa62fe36ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
4e3b2355-3a7a-40e8-81f8-feaa62fe36ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
4e3b2355-3a7a-40e8-81f8-feaa62fe36ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
4e3b2355-3a7a-40e8-81f8-feaa62fe36ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
4e3b2355-3a7a-40e8-81f8-feaa62fe36ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
4e3b2355-3a7a-40e8-81f8-feaa62fe36ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
4e3b2355-3a7a-40e8-81f8-feaa62fe36ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
4e3b2355-3a7a-40e8-81f8-feaa62fe36ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
4e3b2355-3a7a-40e8-81f8-feaa62fe36ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
4e3b2355-3a7a-40e8-81f8-feaa62fe36ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
4e3b2355-3a7a-40e8-81f8-feaa62fe36ee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.",True,USMLE,Figure 1.1,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.1-300x133.png,Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.
c9b8d9ef-46ae-4be9-a3f0-b8a992b66dfa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,10q22,False,10q22,,,,
a6b7f4e5-8455-4193-8c6a-1c8e63e7b966,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,q24,False,q24,,,,
5dd6c928-2286-4400-aacf-459c9d801d02,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,fibrillatory,False,fibrillatory,,,,
34a359db-cc02-465e-8e0b-a6d6f58f2a7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
34a359db-cc02-465e-8e0b-a6d6f58f2a7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
34a359db-cc02-465e-8e0b-a6d6f58f2a7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
34a359db-cc02-465e-8e0b-a6d6f58f2a7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
34a359db-cc02-465e-8e0b-a6d6f58f2a7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
34a359db-cc02-465e-8e0b-a6d6f58f2a7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
34a359db-cc02-465e-8e0b-a6d6f58f2a7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
34a359db-cc02-465e-8e0b-a6d6f58f2a7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
34a359db-cc02-465e-8e0b-a6d6f58f2a7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
34a359db-cc02-465e-8e0b-a6d6f58f2a7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
34a359db-cc02-465e-8e0b-a6d6f58f2a7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
34a359db-cc02-465e-8e0b-a6d6f58f2a7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
34a359db-cc02-465e-8e0b-a6d6f58f2a7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
34a359db-cc02-465e-8e0b-a6d6f58f2a7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
34a359db-cc02-465e-8e0b-a6d6f58f2a7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
34a359db-cc02-465e-8e0b-a6d6f58f2a7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
34a359db-cc02-465e-8e0b-a6d6f58f2a7d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).",True,fibrillatory,Figure 1.2,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.2.png,"Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right)."
90f6721d-1b0d-43fb-8584-aaa0db60155c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Table 1.1: Atrial fibrillation summary.,True,fibrillatory,,,,
26abda3a-e85b-4750-b8ff-3d51179ceadd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Atrial Flutter,False,Atrial Flutter,,,,
ec7f0429-5045-40b7-9a81-4f01f2518fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
ec7f0429-5045-40b7-9a81-4f01f2518fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
ec7f0429-5045-40b7-9a81-4f01f2518fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
ec7f0429-5045-40b7-9a81-4f01f2518fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
ec7f0429-5045-40b7-9a81-4f01f2518fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
ec7f0429-5045-40b7-9a81-4f01f2518fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
ec7f0429-5045-40b7-9a81-4f01f2518fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
ec7f0429-5045-40b7-9a81-4f01f2518fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
ec7f0429-5045-40b7-9a81-4f01f2518fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
ec7f0429-5045-40b7-9a81-4f01f2518fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
ec7f0429-5045-40b7-9a81-4f01f2518fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
ec7f0429-5045-40b7-9a81-4f01f2518fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
ec7f0429-5045-40b7-9a81-4f01f2518fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
ec7f0429-5045-40b7-9a81-4f01f2518fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
ec7f0429-5045-40b7-9a81-4f01f2518fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
ec7f0429-5045-40b7-9a81-4f01f2518fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
ec7f0429-5045-40b7-9a81-4f01f2518fdc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).",True,Atrial Flutter,Figure 1.3,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.3-new.jpg,Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.
28905f72-664a-4084-8c99-8f018d84d7d0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,macroreentrant,False,macroreentrant,,,,
204915c4-6bdf-4ad4-8dd9-331e38b49daa,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,cavotricuspid,False,cavotricuspid,,,,
17d3ea9b-9366-4c26-899f-53620cb0ab30,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"As with atrial fibrillation, the AV node’s refractory period prevents most of the P-waves from progressing to the ventricle, but commonly the AV conduction will be 2-to-1, so with an atrial rate of 300 bpm the ventricular rate will be 150 bpm. Parasympathetic stimulation or changes in AV node refractoriness can modify how many P-waves pass into the ventricle, but the the resultant rhythm is “regularly irregular.” When the heart rate is elevated, then distinguishing flutter from fibrillation becomes challenging and slowing ventricular rate pharmaceutically (adenosine) helps the flutter waves reemerge for a definitive diagnosis to be made.",True,cavotricuspid,,,,
680a38de-243b-4770-9555-995a454f9027,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Table 1.2: Atrial flutter summary.,True,cavotricuspid,,,,
a192ed34-83b3-4399-9c38-6142bb5417fc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Multifocal Atrial Tachycardia,False,Multifocal Atrial Tachycardia,,,,
a05512b8-9559-463e-acae-30a20fb28b9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a05512b8-9559-463e-acae-30a20fb28b9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a05512b8-9559-463e-acae-30a20fb28b9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a05512b8-9559-463e-acae-30a20fb28b9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a05512b8-9559-463e-acae-30a20fb28b9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a05512b8-9559-463e-acae-30a20fb28b9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a05512b8-9559-463e-acae-30a20fb28b9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a05512b8-9559-463e-acae-30a20fb28b9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a05512b8-9559-463e-acae-30a20fb28b9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a05512b8-9559-463e-acae-30a20fb28b9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a05512b8-9559-463e-acae-30a20fb28b9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a05512b8-9559-463e-acae-30a20fb28b9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a05512b8-9559-463e-acae-30a20fb28b9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a05512b8-9559-463e-acae-30a20fb28b9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a05512b8-9559-463e-acae-30a20fb28b9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a05512b8-9559-463e-acae-30a20fb28b9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
a05512b8-9559-463e-acae-30a20fb28b9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.",True,Multifocal Atrial Tachycardia,Figure 1.4,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.4-scaled.jpg,Figure 1.4: Three distinct P-wave morphologies in a case of MAT.
aa0560cf-66f7-4517-a301-ae33c6098625,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"MAT frequently occurs in the setting of severe lung disease and, more specifically, during an exacerbation of lung disease. This rhythm is benign, and once the underlying lung disease is treated, it should resolve.",True,Multifocal Atrial Tachycardia,,,,
5c1a367c-e9bf-48b1-8145-2e3679d2c14d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Table 1.3: MAT summary.,True,Multifocal Atrial Tachycardia,,,,
4b4ed59b-9cd6-4342-8c81-f68f15c4ef81,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Premature Atrial Contraction,False,Premature Atrial Contraction,,,,
c2fe886a-b2c6-4b9e-8477-1a843361c28f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A premature atrial contraction (PAC) is generated by a depolarization instigated outside of the SA node. This produces an extra P-wave, and consequently a shortening from previous P-P intervals is seen. The aberrant P-wave also has a different morphology from a sinus P-wave because of its different anatomical origin.",True,Premature Atrial Contraction,,,,
49f80fff-eb5b-400e-ad97-42f8918f1981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
49f80fff-eb5b-400e-ad97-42f8918f1981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
49f80fff-eb5b-400e-ad97-42f8918f1981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
49f80fff-eb5b-400e-ad97-42f8918f1981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
49f80fff-eb5b-400e-ad97-42f8918f1981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
49f80fff-eb5b-400e-ad97-42f8918f1981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
49f80fff-eb5b-400e-ad97-42f8918f1981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
49f80fff-eb5b-400e-ad97-42f8918f1981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
49f80fff-eb5b-400e-ad97-42f8918f1981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
49f80fff-eb5b-400e-ad97-42f8918f1981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
49f80fff-eb5b-400e-ad97-42f8918f1981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
49f80fff-eb5b-400e-ad97-42f8918f1981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
49f80fff-eb5b-400e-ad97-42f8918f1981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
49f80fff-eb5b-400e-ad97-42f8918f1981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
49f80fff-eb5b-400e-ad97-42f8918f1981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
49f80fff-eb5b-400e-ad97-42f8918f1981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
49f80fff-eb5b-400e-ad97-42f8918f1981,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).",True,Premature Atrial Contraction,Figure 1.5,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.5.png,Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
090e4615-a93e-42d8-a27d-1f5b97e6d0ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"If a PAC occurs when the AV node has not yet recovered from its refractory period, the PAC will fail to conduct to the ventricles; meaning the PAC will not be followed by a QRS complex or the ectopic P-R interval will be prolonged. The ECG will show a premature, ectopic P-wave and then no QRS complex afterward. When this occurs along with bigeminy, the ECG can appear as if there is sinus bradycardia.",True,Premature Atrial Contraction,,,,
95f5d196-510f-421a-9c0c-0a4ae79c4cbc,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Table 1.4: PAC summary.,True,Premature Atrial Contraction,,,,
e430b674-ce3c-4e30-807c-2ed98606c11d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Sinus Bradycardia,False,Sinus Bradycardia,,,,
cea06f07-e26e-4438-9355-e26767abafee,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Sinus bradycardia denotes a sinus rhythm below 60 bpm. Otherwise the ECG waveform is normal on an ECG with an upright P-wave in lead II preceding every QRS complex. There are many intrinsic causes associated with the heart itself, as well as extrinsic causes, some of which are listed table 1.5. Sinus bradycardia is usually asymptomatic as rates of 40–50 bpm can maintain hemodynamic stability. Rates below this can produce symptoms of fatigue, dizziness, and dyspnea on exertion.",True,Sinus Bradycardia,,,,
4a2fad9f-e995-454b-895e-96cb6a2fc5b4,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Table 1.5: Intrinsic and extrinsic causes associated with the heart.,True,Sinus Bradycardia,,,,
14f63ce6-e2f3-4cf7-9af7-bd35c4a0db58,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Table 1.6: Sinus bradycardia summary.,True,Sinus Bradycardia,,,,
b22d40e3-b209-4b61-ad27-c6ada14103d9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Premature Ventricular Contractions,False,Premature Ventricular Contractions,,,,
3e70f438-7fc5-42bd-8b14-6d924068a89b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e70f438-7fc5-42bd-8b14-6d924068a89b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e70f438-7fc5-42bd-8b14-6d924068a89b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e70f438-7fc5-42bd-8b14-6d924068a89b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e70f438-7fc5-42bd-8b14-6d924068a89b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e70f438-7fc5-42bd-8b14-6d924068a89b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e70f438-7fc5-42bd-8b14-6d924068a89b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e70f438-7fc5-42bd-8b14-6d924068a89b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e70f438-7fc5-42bd-8b14-6d924068a89b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e70f438-7fc5-42bd-8b14-6d924068a89b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e70f438-7fc5-42bd-8b14-6d924068a89b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e70f438-7fc5-42bd-8b14-6d924068a89b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e70f438-7fc5-42bd-8b14-6d924068a89b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e70f438-7fc5-42bd-8b14-6d924068a89b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e70f438-7fc5-42bd-8b14-6d924068a89b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e70f438-7fc5-42bd-8b14-6d924068a89b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
3e70f438-7fc5-42bd-8b14-6d924068a89b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).",True,Premature Ventricular Contractions,Figure 1.6,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.6-bw.png,Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
f2320a30-2682-4072-98eb-5414193c4c41,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Table 1.7: PVC summary.,True,Premature Ventricular Contractions,,,,
f8b564ea-2119-48d5-a4ca-5485e538f95f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Ventricular Tachycardia,False,Ventricular Tachycardia,,,,
d2849711-56e2-4315-8123-556f2d734527,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Ventricular tachycardia (VT) is caused by reentry currents being established in the ventricular myocardium or groups of ventricular myocytes that have aberrant electrical behavior. As such, VT is usually caused by underlying cardiac disease.",True,Ventricular Tachycardia,,,,
b1cb8997-7536-4b02-8039-0175ddc12e66,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Like a PVC, the aberrant depolarizations do not follow the normal conduction pathways so are wide (>120 msecs), but unlike a PVC, VT involves a ventricular rate >100 bpm. With disorganized contractility and reduced filling time, VT can lead to hemodynamic instability and severe hypotension—hence it is life threatening.",True,Ventricular Tachycardia,,,,
0abfae8d-05d9-45a3-8b29-853543031741,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The QRS morphology in VT is highly variable between patients and depends on where the arrhythmia originates. Consequently there are several ways to classify VT based on duration, symptoms, QRS morphology, rate, and origin.",True,Ventricular Tachycardia,,,,
b26f0f1a-6485-4ca4-8248-ef4b62a660d3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Sustained VT is any VT that lasts for more than 30 seconds or is symptomatic. Nonsustained VT lasts for less than 30 seconds and is asymptomatic.,True,Ventricular Tachycardia,,,,
7569b91a-3437-43ef-922e-f05d4051c88c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
7569b91a-3437-43ef-922e-f05d4051c88c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
7569b91a-3437-43ef-922e-f05d4051c88c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
7569b91a-3437-43ef-922e-f05d4051c88c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
7569b91a-3437-43ef-922e-f05d4051c88c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
7569b91a-3437-43ef-922e-f05d4051c88c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
7569b91a-3437-43ef-922e-f05d4051c88c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
7569b91a-3437-43ef-922e-f05d4051c88c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
7569b91a-3437-43ef-922e-f05d4051c88c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
7569b91a-3437-43ef-922e-f05d4051c88c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
7569b91a-3437-43ef-922e-f05d4051c88c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
7569b91a-3437-43ef-922e-f05d4051c88c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
7569b91a-3437-43ef-922e-f05d4051c88c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
7569b91a-3437-43ef-922e-f05d4051c88c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
7569b91a-3437-43ef-922e-f05d4051c88c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
7569b91a-3437-43ef-922e-f05d4051c88c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
7569b91a-3437-43ef-922e-f05d4051c88c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.,True,Ventricular Tachycardia,Figure 1.7,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.7-new-scaled.jpg,Figure 1.7: Monomorphic and polymorphic VT.
b5e46cd4-3a74-4ab3-bec3-1b1a19b0f938,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
b5e46cd4-3a74-4ab3-bec3-1b1a19b0f938,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
b5e46cd4-3a74-4ab3-bec3-1b1a19b0f938,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
b5e46cd4-3a74-4ab3-bec3-1b1a19b0f938,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
b5e46cd4-3a74-4ab3-bec3-1b1a19b0f938,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
b5e46cd4-3a74-4ab3-bec3-1b1a19b0f938,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
b5e46cd4-3a74-4ab3-bec3-1b1a19b0f938,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
b5e46cd4-3a74-4ab3-bec3-1b1a19b0f938,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
b5e46cd4-3a74-4ab3-bec3-1b1a19b0f938,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
b5e46cd4-3a74-4ab3-bec3-1b1a19b0f938,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
b5e46cd4-3a74-4ab3-bec3-1b1a19b0f938,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
b5e46cd4-3a74-4ab3-bec3-1b1a19b0f938,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
b5e46cd4-3a74-4ab3-bec3-1b1a19b0f938,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
b5e46cd4-3a74-4ab3-bec3-1b1a19b0f938,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
b5e46cd4-3a74-4ab3-bec3-1b1a19b0f938,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
b5e46cd4-3a74-4ab3-bec3-1b1a19b0f938,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
b5e46cd4-3a74-4ab3-bec3-1b1a19b0f938,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).",True,Ventricular Tachycardia,Figure 1.8,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.8-scaled.jpg,Figure 1.8: Torsades de pointes.
46397c9c-db3f-49d6-909d-e7700b61d49b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Torsades de pointes is associated with a prolonged QT interval (>600 msecs) that helps distinguish it from other forms of polymorphous VT. The longer QT interval can be caused by ionic abnormalities that reduce the repolarizing current of Phase 3 of the cardiac action potential. This makes the myocardium susceptible to early after-depolarizations—the trigger for torsades de pointes. These after-depolarizations do not happen uniformly across the myocardium and are more common in endocardial tissue where the repolarization currents are slower. So torsades de pointes arises from the after-depolarizations causing reentry currents in neighboring tissue.,True,Ventricular Tachycardia,,,,
1f657369-541b-4fbe-b32f-59b6e7984599,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Both common garden variety VTs and torsades de pointes can progress to ventricular fibrillation.,True,Ventricular Tachycardia,,,,
69c0c87f-dc75-4791-bf17-05a008de4a72,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Table 1.8: VT summary.,True,Ventricular Tachycardia,,,,
1478d855-cb19-4d23-b0e4-f569133361bb,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Ventricular Fibrillation,False,Ventricular Fibrillation,,,,
880b5e9b-1824-4e10-9eb9-48e41c40d307,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Ventricular fibrillation (VF) occurs when the ventricular rate exceeds 400 bpm. The disorganized and uncoordinated contraction of the myocardium causes cardiac output to fall to catastrophic levels. Rates of survival for out-of-hospital VF are low.,True,Ventricular Fibrillation,,,,
e7e907f5-7185-4c77-8bdb-59fc7524ce04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
e7e907f5-7185-4c77-8bdb-59fc7524ce04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
e7e907f5-7185-4c77-8bdb-59fc7524ce04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
e7e907f5-7185-4c77-8bdb-59fc7524ce04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
e7e907f5-7185-4c77-8bdb-59fc7524ce04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
e7e907f5-7185-4c77-8bdb-59fc7524ce04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
e7e907f5-7185-4c77-8bdb-59fc7524ce04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
e7e907f5-7185-4c77-8bdb-59fc7524ce04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
e7e907f5-7185-4c77-8bdb-59fc7524ce04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
e7e907f5-7185-4c77-8bdb-59fc7524ce04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
e7e907f5-7185-4c77-8bdb-59fc7524ce04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
e7e907f5-7185-4c77-8bdb-59fc7524ce04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
e7e907f5-7185-4c77-8bdb-59fc7524ce04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
e7e907f5-7185-4c77-8bdb-59fc7524ce04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
e7e907f5-7185-4c77-8bdb-59fc7524ce04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
e7e907f5-7185-4c77-8bdb-59fc7524ce04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
e7e907f5-7185-4c77-8bdb-59fc7524ce04,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.",True,Ventricular Fibrillation,Figure 1.9,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.9.jpeg,Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
c37db57b-bccb-4415-a5fe-8800f1b1cd93,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Table 1.9: VF summary.,True,Ventricular Fibrillation,,,,
4912e3c2-afe1-424d-bbb2-580ec327708f,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,First-Degree Atrioventricular Block,False,First-Degree Atrioventricular Block,,,,
8ec39ec4-a78b-4b58-ba96-ebc48dbf1b9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8ec39ec4-a78b-4b58-ba96-ebc48dbf1b9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8ec39ec4-a78b-4b58-ba96-ebc48dbf1b9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8ec39ec4-a78b-4b58-ba96-ebc48dbf1b9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8ec39ec4-a78b-4b58-ba96-ebc48dbf1b9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8ec39ec4-a78b-4b58-ba96-ebc48dbf1b9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8ec39ec4-a78b-4b58-ba96-ebc48dbf1b9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8ec39ec4-a78b-4b58-ba96-ebc48dbf1b9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8ec39ec4-a78b-4b58-ba96-ebc48dbf1b9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8ec39ec4-a78b-4b58-ba96-ebc48dbf1b9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8ec39ec4-a78b-4b58-ba96-ebc48dbf1b9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8ec39ec4-a78b-4b58-ba96-ebc48dbf1b9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8ec39ec4-a78b-4b58-ba96-ebc48dbf1b9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8ec39ec4-a78b-4b58-ba96-ebc48dbf1b9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8ec39ec4-a78b-4b58-ba96-ebc48dbf1b9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8ec39ec4-a78b-4b58-ba96-ebc48dbf1b9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
8ec39ec4-a78b-4b58-ba96-ebc48dbf1b9a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f8daf407-335d-4141-9723-1f63cc653cf7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f8daf407-335d-4141-9723-1f63cc653cf7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f8daf407-335d-4141-9723-1f63cc653cf7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f8daf407-335d-4141-9723-1f63cc653cf7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f8daf407-335d-4141-9723-1f63cc653cf7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f8daf407-335d-4141-9723-1f63cc653cf7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f8daf407-335d-4141-9723-1f63cc653cf7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f8daf407-335d-4141-9723-1f63cc653cf7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f8daf407-335d-4141-9723-1f63cc653cf7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f8daf407-335d-4141-9723-1f63cc653cf7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f8daf407-335d-4141-9723-1f63cc653cf7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f8daf407-335d-4141-9723-1f63cc653cf7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f8daf407-335d-4141-9723-1f63cc653cf7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f8daf407-335d-4141-9723-1f63cc653cf7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f8daf407-335d-4141-9723-1f63cc653cf7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f8daf407-335d-4141-9723-1f63cc653cf7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
f8daf407-335d-4141-9723-1f63cc653cf7,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.",True,First-Degree Atrioventricular Block,Figure 1.10,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.10-scaled.jpg,Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.
43ca2e9e-f9b5-4283-8308-8a11d55e159e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Table 1.10: First-degree block summary.,True,First-Degree Atrioventricular Block,,,,
ec0a73d0-a206-4b10-92c9-1bbd12489ed3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Second-Degree Atrioventricular Block,False,Second-Degree Atrioventricular Block,,,,
bbef0a21-6161-450b-bf2d-fac3f1c0b925,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A second-degree atrioventricular block also has changes in P-R interval, but it starts to show failure of the P-wave to propagate a QRS complex every time (i.e., intermittently the depolarization fails to reach the ventricles). The pattern of missed ventricular depolarizations, or blocked P-waves, is often very regular and described as a ratio of P-waves to QRS complex. The way in which the P-R interval changes in relation to the blocked P-waves produces subclassifications of second-degree blocks, Mobitz I and II.",True,Second-Degree Atrioventricular Block,,,,
e904692d-4498-4d2f-8985-8dbb1d1c7fe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
e904692d-4498-4d2f-8985-8dbb1d1c7fe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
e904692d-4498-4d2f-8985-8dbb1d1c7fe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
e904692d-4498-4d2f-8985-8dbb1d1c7fe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
e904692d-4498-4d2f-8985-8dbb1d1c7fe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
e904692d-4498-4d2f-8985-8dbb1d1c7fe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
e904692d-4498-4d2f-8985-8dbb1d1c7fe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
e904692d-4498-4d2f-8985-8dbb1d1c7fe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
e904692d-4498-4d2f-8985-8dbb1d1c7fe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
e904692d-4498-4d2f-8985-8dbb1d1c7fe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
e904692d-4498-4d2f-8985-8dbb1d1c7fe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
e904692d-4498-4d2f-8985-8dbb1d1c7fe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
e904692d-4498-4d2f-8985-8dbb1d1c7fe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
e904692d-4498-4d2f-8985-8dbb1d1c7fe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
e904692d-4498-4d2f-8985-8dbb1d1c7fe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
e904692d-4498-4d2f-8985-8dbb1d1c7fe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
e904692d-4498-4d2f-8985-8dbb1d1c7fe9,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.,True,Second-Degree Atrioventricular Block,Figure 1.11,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.11-scaled.jpg,Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.
41c6678d-1386-4154-b4a8-0fd7f8d2823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
41c6678d-1386-4154-b4a8-0fd7f8d2823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
41c6678d-1386-4154-b4a8-0fd7f8d2823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
41c6678d-1386-4154-b4a8-0fd7f8d2823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
41c6678d-1386-4154-b4a8-0fd7f8d2823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
41c6678d-1386-4154-b4a8-0fd7f8d2823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
41c6678d-1386-4154-b4a8-0fd7f8d2823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
41c6678d-1386-4154-b4a8-0fd7f8d2823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
41c6678d-1386-4154-b4a8-0fd7f8d2823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
41c6678d-1386-4154-b4a8-0fd7f8d2823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
41c6678d-1386-4154-b4a8-0fd7f8d2823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
41c6678d-1386-4154-b4a8-0fd7f8d2823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
41c6678d-1386-4154-b4a8-0fd7f8d2823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
41c6678d-1386-4154-b4a8-0fd7f8d2823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
41c6678d-1386-4154-b4a8-0fd7f8d2823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
41c6678d-1386-4154-b4a8-0fd7f8d2823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
41c6678d-1386-4154-b4a8-0fd7f8d2823d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.",True,Second-Degree Atrioventricular Block,Figure 1.12,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.12-scaled.jpg,"Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1."
cf3c4cc4-6571-4597-9dfe-9c9b78c271df,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Table 1.11: Second-degree block summary.,True,Second-Degree Atrioventricular Block,,,,
d454eef5-6d2c-40e6-86bd-f439ec0b9814,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Third-Degree Atrioventricular Block,False,Third-Degree Atrioventricular Block,,,,
513da897-b7c9-41ad-bc8d-1ecb60ba9c4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
513da897-b7c9-41ad-bc8d-1ecb60ba9c4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
513da897-b7c9-41ad-bc8d-1ecb60ba9c4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
513da897-b7c9-41ad-bc8d-1ecb60ba9c4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
513da897-b7c9-41ad-bc8d-1ecb60ba9c4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
513da897-b7c9-41ad-bc8d-1ecb60ba9c4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
513da897-b7c9-41ad-bc8d-1ecb60ba9c4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
513da897-b7c9-41ad-bc8d-1ecb60ba9c4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
513da897-b7c9-41ad-bc8d-1ecb60ba9c4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
513da897-b7c9-41ad-bc8d-1ecb60ba9c4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
513da897-b7c9-41ad-bc8d-1ecb60ba9c4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
513da897-b7c9-41ad-bc8d-1ecb60ba9c4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
513da897-b7c9-41ad-bc8d-1ecb60ba9c4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
513da897-b7c9-41ad-bc8d-1ecb60ba9c4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
513da897-b7c9-41ad-bc8d-1ecb60ba9c4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
513da897-b7c9-41ad-bc8d-1ecb60ba9c4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
513da897-b7c9-41ad-bc8d-1ecb60ba9c4b,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.",True,Third-Degree Atrioventricular Block,Figure 1.13,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.13-1-scaled.jpg,Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
65693727-e09c-42ba-84d3-aba97ae61b0a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Table 1.12: Third-degree block summary.,True,Third-Degree Atrioventricular Block,,,,
06efe10a-d2e9-4cd8-831b-8778d5eba075,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Left Bundle Branch Block,False,Left Bundle Branch Block,,,,
f2b5b129-c78d-42ba-8266-da3b99141f92,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"A left bundle branch block (LBBB) is generated when the conductivity of the His-Purkinje system in the left ventricle is compromised, either through damage or disease. The ECG changes, and criteria for LBBB relate to these changes in conductivity and the left-side location.",True,Left Bundle Branch Block,,,,
aa072545-00c5-4213-bb83-acebea5890e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
aa072545-00c5-4213-bb83-acebea5890e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
aa072545-00c5-4213-bb83-acebea5890e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
aa072545-00c5-4213-bb83-acebea5890e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
aa072545-00c5-4213-bb83-acebea5890e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
aa072545-00c5-4213-bb83-acebea5890e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
aa072545-00c5-4213-bb83-acebea5890e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
aa072545-00c5-4213-bb83-acebea5890e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
aa072545-00c5-4213-bb83-acebea5890e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
aa072545-00c5-4213-bb83-acebea5890e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
aa072545-00c5-4213-bb83-acebea5890e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
aa072545-00c5-4213-bb83-acebea5890e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
aa072545-00c5-4213-bb83-acebea5890e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
aa072545-00c5-4213-bb83-acebea5890e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
aa072545-00c5-4213-bb83-acebea5890e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
aa072545-00c5-4213-bb83-acebea5890e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
aa072545-00c5-4213-bb83-acebea5890e1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
26ef182e-35c8-48f1-91e0-f68e287ada80,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The lateral leads (I, V5, and V6) normally show a downward deflecting Q-wave as normal septal deflection initially occurs left-to-right (i.e., away from the lateral leads). In LBBB the change in direction to right-to-left, plus the longer duration, eliminates the Q-wave from the lateral leads, and Q-waves will be small in aVL.",True,Left Bundle Branch Block,,,,
770c0c44-d224-464e-a575-e6b30d39d543,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
770c0c44-d224-464e-a575-e6b30d39d543,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
770c0c44-d224-464e-a575-e6b30d39d543,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
770c0c44-d224-464e-a575-e6b30d39d543,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
770c0c44-d224-464e-a575-e6b30d39d543,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
770c0c44-d224-464e-a575-e6b30d39d543,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
770c0c44-d224-464e-a575-e6b30d39d543,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
770c0c44-d224-464e-a575-e6b30d39d543,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
770c0c44-d224-464e-a575-e6b30d39d543,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
770c0c44-d224-464e-a575-e6b30d39d543,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
770c0c44-d224-464e-a575-e6b30d39d543,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
770c0c44-d224-464e-a575-e6b30d39d543,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
770c0c44-d224-464e-a575-e6b30d39d543,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
770c0c44-d224-464e-a575-e6b30d39d543,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
770c0c44-d224-464e-a575-e6b30d39d543,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
770c0c44-d224-464e-a575-e6b30d39d543,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
770c0c44-d224-464e-a575-e6b30d39d543,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).,True,Left Bundle Branch Block,Figure 1.15,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.15.png,Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.
068c1096-1f88-4f96-9eb6-b3910df25b37,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
068c1096-1f88-4f96-9eb6-b3910df25b37,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
068c1096-1f88-4f96-9eb6-b3910df25b37,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
068c1096-1f88-4f96-9eb6-b3910df25b37,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
068c1096-1f88-4f96-9eb6-b3910df25b37,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
068c1096-1f88-4f96-9eb6-b3910df25b37,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
068c1096-1f88-4f96-9eb6-b3910df25b37,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
068c1096-1f88-4f96-9eb6-b3910df25b37,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
068c1096-1f88-4f96-9eb6-b3910df25b37,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
068c1096-1f88-4f96-9eb6-b3910df25b37,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
068c1096-1f88-4f96-9eb6-b3910df25b37,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
068c1096-1f88-4f96-9eb6-b3910df25b37,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
068c1096-1f88-4f96-9eb6-b3910df25b37,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
068c1096-1f88-4f96-9eb6-b3910df25b37,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
068c1096-1f88-4f96-9eb6-b3910df25b37,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
068c1096-1f88-4f96-9eb6-b3910df25b37,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
068c1096-1f88-4f96-9eb6-b3910df25b37,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).",True,Left Bundle Branch Block,Figure 1.14,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.14-scaled.jpg,Figure 1.14: Example of LBBB with defining features labeled.
2f89fc47-6a04-4b3a-a9b0-70b5cd4c19a2,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Table 1.13: LBBB summary.,True,Left Bundle Branch Block,,,,
28d9bf6a-15f8-45f8-8b5e-781c07a3ae2c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Right Bundle Branch Block,False,Right Bundle Branch Block,,,,
cb1fc2c9-9124-488b-9eb5-dd45634546bd,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The causes and manifestations of a right bundle branch block (RBBB) bear some similarities to those described for LBBB, but of course this time its depolarization of the right ventricle is delayed. Causes of RBBB include ischemic heart disease again as well as other myocardial diseases, but pulmonary issues such as pulmonary embolism and cor pulmonale can be added to the list.",True,Right Bundle Branch Block,,,,
74a54d75-3856-4fb4-b581-82a5667809c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
74a54d75-3856-4fb4-b581-82a5667809c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
74a54d75-3856-4fb4-b581-82a5667809c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
74a54d75-3856-4fb4-b581-82a5667809c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
74a54d75-3856-4fb4-b581-82a5667809c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
74a54d75-3856-4fb4-b581-82a5667809c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
74a54d75-3856-4fb4-b581-82a5667809c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
74a54d75-3856-4fb4-b581-82a5667809c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
74a54d75-3856-4fb4-b581-82a5667809c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
74a54d75-3856-4fb4-b581-82a5667809c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
74a54d75-3856-4fb4-b581-82a5667809c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
74a54d75-3856-4fb4-b581-82a5667809c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
74a54d75-3856-4fb4-b581-82a5667809c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
74a54d75-3856-4fb4-b581-82a5667809c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
74a54d75-3856-4fb4-b581-82a5667809c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
74a54d75-3856-4fb4-b581-82a5667809c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
74a54d75-3856-4fb4-b581-82a5667809c5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).",True,Right Bundle Branch Block,Figure 1.16,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.16-scaled.jpg,Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.
b1e1f113-e7a6-46f1-83ee-88353339b7fe,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Table 1.14: RBBB summary.,True,Right Bundle Branch Block,,,,
fca749c4-34ed-4b7b-be96-58aa7a6e4f73,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Wolff-Parkinson-White Syndrome,False,Wolff-Parkinson-White Syndrome,,,,
251fedfb-3d26-4410-8f3e-81606a7089b0,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Normally the only electrical connection between the atria and the ventricles is the AV node. Otherwise the fibrous skeleton of the heart electrically insulates the atria from the ventricles. In Wolff-Parkinson-White (WPW) syndrome, that insulation is incomplete, and an “accessory pathway” connects the electrical system of the atria directly to the ventricles. If you think of the AV node as a bridge over the fibrous wall with regulated access, the accessory pathway is like a pathological tunnel under it with no regulation.",True,Wolff-Parkinson-White Syndrome,,,,
45e38867-c343-4113-ac73-4cd882844dad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
45e38867-c343-4113-ac73-4cd882844dad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
45e38867-c343-4113-ac73-4cd882844dad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
45e38867-c343-4113-ac73-4cd882844dad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
45e38867-c343-4113-ac73-4cd882844dad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
45e38867-c343-4113-ac73-4cd882844dad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
45e38867-c343-4113-ac73-4cd882844dad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
45e38867-c343-4113-ac73-4cd882844dad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
45e38867-c343-4113-ac73-4cd882844dad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
45e38867-c343-4113-ac73-4cd882844dad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
45e38867-c343-4113-ac73-4cd882844dad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
45e38867-c343-4113-ac73-4cd882844dad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
45e38867-c343-4113-ac73-4cd882844dad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
45e38867-c343-4113-ac73-4cd882844dad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
45e38867-c343-4113-ac73-4cd882844dad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
45e38867-c343-4113-ac73-4cd882844dad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
45e38867-c343-4113-ac73-4cd882844dad,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).",True,Wolff-Parkinson-White Syndrome,Figure 1.17,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.17-new.png,Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
16bd0e2b-412b-42e0-ae00-b20e1f191c6d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"WPW syndrome is often asymptomatic, and patients do not require immediate treatment. However, if atrial fibrillation occurs in a WPW patient, the accessory pathway can allow the atrial fibrillation waves through to the ventricle (with no AV nodal refractory period to prevent them). Consequently a high ventricular rate is seen, and the risk of ventricular fibrillation being established means immediate clinical attention is required.",True,Wolff-Parkinson-White Syndrome,,,,
1f228197-6d65-4cc4-8535-c937152cbe23,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Hyper- and Hypocalcemia,False,Hyper- and Hypocalcemia,,,,
938f80c5-4a89-49e8-a979-9cd74db2cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
938f80c5-4a89-49e8-a979-9cd74db2cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
938f80c5-4a89-49e8-a979-9cd74db2cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
938f80c5-4a89-49e8-a979-9cd74db2cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
938f80c5-4a89-49e8-a979-9cd74db2cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
938f80c5-4a89-49e8-a979-9cd74db2cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
938f80c5-4a89-49e8-a979-9cd74db2cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
938f80c5-4a89-49e8-a979-9cd74db2cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
938f80c5-4a89-49e8-a979-9cd74db2cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
938f80c5-4a89-49e8-a979-9cd74db2cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
938f80c5-4a89-49e8-a979-9cd74db2cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
938f80c5-4a89-49e8-a979-9cd74db2cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
938f80c5-4a89-49e8-a979-9cd74db2cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
938f80c5-4a89-49e8-a979-9cd74db2cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
938f80c5-4a89-49e8-a979-9cd74db2cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
938f80c5-4a89-49e8-a979-9cd74db2cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
938f80c5-4a89-49e8-a979-9cd74db2cc54,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.19,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.19-scaled.jpg,Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
d4313d1f-3cac-44c9-9ce8-fd7bbe6670af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
d4313d1f-3cac-44c9-9ce8-fd7bbe6670af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
d4313d1f-3cac-44c9-9ce8-fd7bbe6670af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
d4313d1f-3cac-44c9-9ce8-fd7bbe6670af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
d4313d1f-3cac-44c9-9ce8-fd7bbe6670af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
d4313d1f-3cac-44c9-9ce8-fd7bbe6670af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
d4313d1f-3cac-44c9-9ce8-fd7bbe6670af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
d4313d1f-3cac-44c9-9ce8-fd7bbe6670af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
d4313d1f-3cac-44c9-9ce8-fd7bbe6670af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
d4313d1f-3cac-44c9-9ce8-fd7bbe6670af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
d4313d1f-3cac-44c9-9ce8-fd7bbe6670af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
d4313d1f-3cac-44c9-9ce8-fd7bbe6670af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
d4313d1f-3cac-44c9-9ce8-fd7bbe6670af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
d4313d1f-3cac-44c9-9ce8-fd7bbe6670af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
d4313d1f-3cac-44c9-9ce8-fd7bbe6670af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
d4313d1f-3cac-44c9-9ce8-fd7bbe6670af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
d4313d1f-3cac-44c9-9ce8-fd7bbe6670af,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).",True,Hyper- and Hypocalcemia,Figure 1.20,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.20-scaled.jpg,Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.
6dd5a1c6-f6cf-4a8e-baa7-be6016f7809d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Table 1.16: Hyper- and hypocalcemia summary.,True,Hyper- and Hypocalcemia,,,,
fc0db523-4da4-48b9-956e-6037d3945dab,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Hyper- and Hypokalemia,False,Hyper- and Hypokalemia,,,,
5c83e93d-0aa9-4705-879b-769888c6a99d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"The pathophysiology is not as simple as changes in extracellular K+ changing the electrochemical gradient for K+. Because of potassium’s role in maintaining the resting membrane potential, shifts in extracellular potassium can also influence the activity of Na+ and Ca++ channels.",True,Hyper- and Hypokalemia,,,,
f03f04c5-a1fd-4a6b-a42a-4ae9de9f929c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
f03f04c5-a1fd-4a6b-a42a-4ae9de9f929c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
f03f04c5-a1fd-4a6b-a42a-4ae9de9f929c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
f03f04c5-a1fd-4a6b-a42a-4ae9de9f929c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
f03f04c5-a1fd-4a6b-a42a-4ae9de9f929c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
f03f04c5-a1fd-4a6b-a42a-4ae9de9f929c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
f03f04c5-a1fd-4a6b-a42a-4ae9de9f929c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
f03f04c5-a1fd-4a6b-a42a-4ae9de9f929c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
f03f04c5-a1fd-4a6b-a42a-4ae9de9f929c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
f03f04c5-a1fd-4a6b-a42a-4ae9de9f929c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
f03f04c5-a1fd-4a6b-a42a-4ae9de9f929c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
f03f04c5-a1fd-4a6b-a42a-4ae9de9f929c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
f03f04c5-a1fd-4a6b-a42a-4ae9de9f929c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
f03f04c5-a1fd-4a6b-a42a-4ae9de9f929c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
f03f04c5-a1fd-4a6b-a42a-4ae9de9f929c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
f03f04c5-a1fd-4a6b-a42a-4ae9de9f929c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
f03f04c5-a1fd-4a6b-a42a-4ae9de9f929c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.",True,Hyper- and Hypokalemia,Figure 1.21,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.21-scaled.jpg,Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.
5820fee4-0853-4f19-8120-05984ea5304e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"As hypokalemia also inhibits Na+-K+ ATPase, Na+ accumulates inside the cell. This in turn leads to an accumulation of Ca++ because of a subsequent failure of the Na+-Ca++ exchanger. Extended presence of these two positive ions inside the myocyte prolongs the action potential and may manifest as an increased width and amplitude of the P-wave.",True,Hyper- and Hypokalemia,,,,
c412ef1f-5e1c-4e50-a76e-8dcd693221f8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"As hypokalemia worsens, the problems with K+ conductance and repolarization increase, and the myocardium becomes susceptible to early after-depolarization (EAD) arrhythmias.",True,Hyper- and Hypokalemia,,,,
86128ed8-8c9a-4639-bd25-a7ae98e632f1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
86128ed8-8c9a-4639-bd25-a7ae98e632f1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
86128ed8-8c9a-4639-bd25-a7ae98e632f1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
86128ed8-8c9a-4639-bd25-a7ae98e632f1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
86128ed8-8c9a-4639-bd25-a7ae98e632f1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
86128ed8-8c9a-4639-bd25-a7ae98e632f1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
86128ed8-8c9a-4639-bd25-a7ae98e632f1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
86128ed8-8c9a-4639-bd25-a7ae98e632f1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
86128ed8-8c9a-4639-bd25-a7ae98e632f1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
86128ed8-8c9a-4639-bd25-a7ae98e632f1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
86128ed8-8c9a-4639-bd25-a7ae98e632f1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
86128ed8-8c9a-4639-bd25-a7ae98e632f1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
86128ed8-8c9a-4639-bd25-a7ae98e632f1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
86128ed8-8c9a-4639-bd25-a7ae98e632f1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
86128ed8-8c9a-4639-bd25-a7ae98e632f1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
86128ed8-8c9a-4639-bd25-a7ae98e632f1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
86128ed8-8c9a-4639-bd25-a7ae98e632f1,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.",True,Hyper- and Hypokalemia,Figure 1.22,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.22-scaled.jpg,Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.
2af284b3-9591-4ea7-8c88-fdb2cc1c47ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2af284b3-9591-4ea7-8c88-fdb2cc1c47ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2af284b3-9591-4ea7-8c88-fdb2cc1c47ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2af284b3-9591-4ea7-8c88-fdb2cc1c47ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2af284b3-9591-4ea7-8c88-fdb2cc1c47ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2af284b3-9591-4ea7-8c88-fdb2cc1c47ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2af284b3-9591-4ea7-8c88-fdb2cc1c47ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2af284b3-9591-4ea7-8c88-fdb2cc1c47ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2af284b3-9591-4ea7-8c88-fdb2cc1c47ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2af284b3-9591-4ea7-8c88-fdb2cc1c47ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2af284b3-9591-4ea7-8c88-fdb2cc1c47ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2af284b3-9591-4ea7-8c88-fdb2cc1c47ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2af284b3-9591-4ea7-8c88-fdb2cc1c47ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2af284b3-9591-4ea7-8c88-fdb2cc1c47ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2af284b3-9591-4ea7-8c88-fdb2cc1c47ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2af284b3-9591-4ea7-8c88-fdb2cc1c47ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
2af284b3-9591-4ea7-8c88-fdb2cc1c47ec,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).",True,Hyper- and Hypokalemia,Figure 1.23,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.23-scaled.jpg,Figure 1.23: Peaked T-waves with mild hyperkalemia.
e8b525ce-b62d-4036-b8cd-8843ad88398c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e8b525ce-b62d-4036-b8cd-8843ad88398c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e8b525ce-b62d-4036-b8cd-8843ad88398c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e8b525ce-b62d-4036-b8cd-8843ad88398c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e8b525ce-b62d-4036-b8cd-8843ad88398c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e8b525ce-b62d-4036-b8cd-8843ad88398c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e8b525ce-b62d-4036-b8cd-8843ad88398c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e8b525ce-b62d-4036-b8cd-8843ad88398c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e8b525ce-b62d-4036-b8cd-8843ad88398c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e8b525ce-b62d-4036-b8cd-8843ad88398c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e8b525ce-b62d-4036-b8cd-8843ad88398c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e8b525ce-b62d-4036-b8cd-8843ad88398c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e8b525ce-b62d-4036-b8cd-8843ad88398c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e8b525ce-b62d-4036-b8cd-8843ad88398c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e8b525ce-b62d-4036-b8cd-8843ad88398c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e8b525ce-b62d-4036-b8cd-8843ad88398c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
e8b525ce-b62d-4036-b8cd-8843ad88398c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”",True,Hyper- and Hypokalemia,Figure 1.24,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.24-new.jpg,"Figure 1.24: Big T, and little p and r of moderate hyperkalemia."
8a856092-1c7b-4f73-8f2f-982a51aee24e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypokalemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
8a856092-1c7b-4f73-8f2f-982a51aee24e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Hyper- and Hypocalcemia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
8a856092-1c7b-4f73-8f2f-982a51aee24e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Wolff-Parkinson-White Syndrome,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
8a856092-1c7b-4f73-8f2f-982a51aee24e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Right Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
8a856092-1c7b-4f73-8f2f-982a51aee24e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Left Bundle Branch Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
8a856092-1c7b-4f73-8f2f-982a51aee24e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Third-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
8a856092-1c7b-4f73-8f2f-982a51aee24e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Second-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
8a856092-1c7b-4f73-8f2f-982a51aee24e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,First-Degree Atrioventricular Block,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
8a856092-1c7b-4f73-8f2f-982a51aee24e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
8a856092-1c7b-4f73-8f2f-982a51aee24e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Ventricular Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
8a856092-1c7b-4f73-8f2f-982a51aee24e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Ventricular Contractions,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
8a856092-1c7b-4f73-8f2f-982a51aee24e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Sinus Bradycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
8a856092-1c7b-4f73-8f2f-982a51aee24e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Premature Atrial Contraction,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
8a856092-1c7b-4f73-8f2f-982a51aee24e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Multifocal Atrial Tachycardia,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
8a856092-1c7b-4f73-8f2f-982a51aee24e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Flutter,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
8a856092-1c7b-4f73-8f2f-982a51aee24e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,Atrial Fibrillation,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
8a856092-1c7b-4f73-8f2f-982a51aee24e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.",True,Hyper- and Hypokalemia,Figure 1.25,1. Arrhythmias,https://pressbooks.lib.vt.edu/app/uploads/sites/69/2022/03/1.25-new.jpg,Figure 1.25: Preterminal ECG of severe hyperkalemia.
021b9154-532b-487f-8ce3-50c0ea175ee8,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Table 1.17: Hypo- and hyperkalemia summary.,True,Hyper- and Hypokalemia,,,,
1435e7fd-ffed-4f1b-a2b5-9f3bf040947d,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"References, resources, and further reading",False,"References, resources, and further reading",,,,
185d26cf-f367-493d-92fc-fde7b39c96ce,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,Text,False,Text,,,,
ea7f40a1-a917-4489-9965-f296aa845b9e,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Burns, Ed, and Robert Buttner. Hypercalcaemia. Lift in the Fast Lane, 2021. https://litfl.com/hypercalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
cbf4ace4-15b5-4a7a-a62a-ca42b7a0a986,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Burns, Ed, and Robert Buttner. Hypocalcaemia. Life in the Fast Lane, 2021. https://litfl.com/hypocalcaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
aeadf871-37d5-4341-b860-8bb051549742,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Buttner, Robert, and Ed Burns. Hyperkalaemia. Life in the Fast Lane. https://litfl.com/hyperkalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
16f98bd3-10a3-4213-9800-7113670ff712,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Buttner, Robert, and Ed Burns. Hypokalaemia. Life in the Fast Lane, 2021. https://litfl.com/hypokalaemia-ecg-library/, CC BY 4.0.",True,Text,,,,
e32e6223-9980-4393-b2d4-d99a6767ea06,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Chhabra, Lovely, Amandeep Goyal, and Michael D. Benham. Wolff Parkinson White Syndrome. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK554437/, CC BY 4.0.",True,Text,,,,
d14958b8-fc8e-4679-ab06-c5ca948e6e47,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Custer, Adam M., Varun S. Yelamanchili, and Sarah L. Lappin. Multifocal Atrial Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459152/, CC BY 4.0.",True,Text,,,,
59a6a0f2-864d-43c0-9f43-04375096cc32,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Farzam, Khashayar, and John R. Richards. Premature Ventricular Contraction. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532991/, CC BY 4.0.",True,Text,,,,
d665d96d-6dd8-4832-b37e-9cae61f3f29c,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Foth, Christopher, Manesh Kumar Gangwani, and Heidi Alvey. Ventricular Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532954/, CC BY 4.0.",True,Text,,,,
bb384208-bcb8-4d76-975a-452098d3ffd5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Hafeez, Yamama, and Shamai A. Grossman. Sinus Bradycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK493201/, CC BY 4.0.",True,Text,,,,
81057a16-52f9-4817-af70-a05381a95dd3,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Harkness, Weston T., and Mary Hicks. Right Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK507872/, CC BY 4.0.",True,Text,,,,
5732fa95-f0c3-4b45-b073-55b4b1c8dca5,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Heaton, Joseph, and Srikanth Yandrapalli. Premature Atrial Contractions. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK559204/, CC BY 4.0.",True,Text,,,,
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15f0ee8b-0cc9-4ac8-b666-2d0a7928164a,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/,1. Arrhythmias,https://pressbooks.lib.vt.edu/cardiovascularpathophysiology/chapter/chapter-1-arrhythmias/,"Nesheiwat, Zeid, Amandeep Goyal, and Mandar Jagtap. Atrial Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK526072/, CC BY 4.0.",True,Text,,,,
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